It is truly remarkable that although ECG changes were first recognized as markers for ischaemia in 1918, today we are still discovering that there is more to learn in this area.
Changes of ST-Segment
Normal Exercise Electrocardiogram ST and J Point
As the heart rate increases with exercise, a number of predictable changes occur in a normal ECG tracing. The PR-interval is shortened after 1 minute of exercise. The P-wave becomes taller and the Ta wave (wave of atrial repolarisation) increases, resulting in downward displacement of the PQ junction. This is particularly important because the so called baseline, for terms of evaluating ST-segment change, is below that usually considered to be isoelectric tracing. With exercise, the Ta wave tends to extend through the QRS and may influence that junction between the ST-segment and the T-wave.
Prognostic Significance
Asymptomatic patient-Abnormal test prevalence 5 to 12 per cent. Risk of event–9 times greater in abnormal test. 2 per cent event rate (angina) over 4 year follow up. BLS study – with risk factors- elderly patient – event rate varies 3.5 per cent to19 per cent in 9 years follow up. Females- 15 per cent to 20 per cent prevalence-less prognostic value.
Symptomatic Patient: Case Study
First stage positive: 5 per cent annual mortality, Low risk group: < 1 per cent annual mortality. It has become standard practice to use the line of PQ or PR junction as a marker for the baseline when the ST-segment is measured at one fourth the distance between the QRS and peak T in left to right leads, considerable depression is normally seen. The anterior posterior lead changes (V1 to V2) are less prominent than those in the lateral and vertical leads. The absence of significant ST-segment depression in young, vigorous boys and in athletic, middle aged men, suggests that the effect of the Ta wave, can usually be recognized because of the short duration (usually 0.045) of the J point depression.
Upsloping ST-Segment
There are few subjects in exercise literature that has generated more controversy than the significance of up sloping ST-segments. The up sloping ST-segment is considered to indicate ischaemia if, at 80 msec after the J point, the segment is 1.5 mm below the baseline level of the PQ Junction. Junctional changes with very steep up sloping segments are probably not pathological.
Changes of ST-Segment
Normal Exercise Electrocardiogram ST and J Point
As the heart rate increases with exercise, a number of predictable changes occur in a normal ECG tracing. The PR-interval is shortened after 1 minute of exercise. The P-wave becomes taller and the Ta wave (wave of atrial repolarisation) increases, resulting in downward displacement of the PQ junction. This is particularly important because the so called baseline, for terms of evaluating ST-segment change, is below that usually considered to be isoelectric tracing. With exercise, the Ta wave tends to extend through the QRS and may influence that junction between the ST-segment and the T-wave.
Prognostic Significance
Asymptomatic patient-Abnormal test prevalence 5 to 12 per cent. Risk of event–9 times greater in abnormal test. 2 per cent event rate (angina) over 4 year follow up. BLS study – with risk factors- elderly patient – event rate varies 3.5 per cent to19 per cent in 9 years follow up. Females- 15 per cent to 20 per cent prevalence-less prognostic value.
Symptomatic Patient: Case Study
First stage positive: 5 per cent annual mortality, Low risk group: < 1 per cent annual mortality. It has become standard practice to use the line of PQ or PR junction as a marker for the baseline when the ST-segment is measured at one fourth the distance between the QRS and peak T in left to right leads, considerable depression is normally seen. The anterior posterior lead changes (V1 to V2) are less prominent than those in the lateral and vertical leads. The absence of significant ST-segment depression in young, vigorous boys and in athletic, middle aged men, suggests that the effect of the Ta wave, can usually be recognized because of the short duration (usually 0.045) of the J point depression.
Upsloping ST-Segment
There are few subjects in exercise literature that has generated more controversy than the significance of up sloping ST-segments. The up sloping ST-segment is considered to indicate ischaemia if, at 80 msec after the J point, the segment is 1.5 mm below the baseline level of the PQ Junction. Junctional changes with very steep up sloping segments are probably not pathological.
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| Horizontal Versus Downsloping ST-Segment |
The physiological basis for the observed ECG abnormalities is complex and may be multifactorial. The magnitude of the stenosis in an artery, estimated by angiography may not accurately predict the amount of restriction in flow, especially when spasm may be induced by exercise. There has been general agreement however, that an increased magnitude of ST-segment depression usually denotes an increased degree of ischaemia. Ekelund reported an almost a three fold increase in cardiac events in patients with the so called strongly positive stress test (ST depression of 2 mm or more). Current criteria accept 1.5 mm of depression of 0.08 msec from the J point even if the ST-segment slopes upward.Mason and associates in the study of a relation observed that reducing the depression of the ST- segment to 0.5 mm increased the sensitivity to 84 per cent but decreased the specifity to 57 per cent. They found that the ST-segments alone at maximum exercise correlated best with an increased LV filling pressure in 90 per cent of patients.
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| Horizontal Vs Down Sloping of ST-Segment |
Downsloping ST-Segment
The long term follow-up information suggests that patients whose ST depression evolves to downsloping have more severe disease than those that do not. Recently it has been reported that downsloping ST depression indicates that a larger area of myocardium is involved and that when the subepicardial muscle as well as the subendocardium is also ischaemic, is usually due to mutivessel disease. Downsloping pattern in V3 and V4 may be due to the additive effects of anterior wall subendocardial ischaemia superimposed on transmural posterior wall ischaemia.
Anterior transmural ischaemia results in ST elevation and would expect transmural posterior wall ischaemia would produce a vector in the same direction as the anterior subendocardial ischaemia process. Thus downsloping ST depression in V3 and V4 probably represents more severe ischaemia than horizontal. It may be a marker for multivessel disease.
ST Depression only on Recovery
Although ST depression during exercise often persists into recovery, it may not manifest until exercise has been terminated. The reasons for this are still not clear but the phenomena have been studied by several investigations. ST depression occurring in recovery only has the same significance as exercise induced ST changes.Time Course of ST Depression It has long been recognized that when ST depression comes on early at low workloads the degree of ischaemia is likely to be more severe. It has long been taught, when ST depression comes on at high workloads, but resolves very quickly after exercise, it constitutes a false positive ST depression. However, it has been found that significant CAD was more common than not, at least in those who were referred for angiography. As might be expected, patients with early onset, late offset ST depression usually had severe disease. Group of patients with resting ST depression increased with exercise, was found to have severe disease. It has often been stated that these patients should not be tested because the results would include a large number of false positives.This might be true if the patients are asymptomatic, but certainly does not pertain to those who have anginal chest pain. It must be cautioned that not all patients with rapid resolution of ST
depression during recovery have normal coronary arteries.
Magnitude of ST Depression
It is intuitive that the magnitude of ST depression should correlate with the degree of the ischaemia. In patients with left main or left main equivalent angiographic changes or with other severe degrees of the ischaemia, the magnitude of ST depression is greater. When 2 mm or more of ST depression is present the probability of left main disease increases. The degree of ST depression at higher workloads depends on what is used for the indication to terminate exercise.If patients are pushed enough, or if they have some degree of left ventricular hypertrophy they may have severe ST depression. If patients with single vessel disease are encouraged to exercise strenuously or if they have some degrees of LVH, they may have very severe ST depression.Bogaty found that in patients with 2 mm or more of ST depression, survival was determined by the duration of exercise on the Bruce protocol, not on the magnitude of depression. Thus the magnitude of ST depression at maximum workload, may not indicate the severity of coronary artery disease. Major ST depression at low workload indicates severe disease.
Distribution of ST Depression
Although it has been recognized for years that lead V4, V5 and V6 are most likely to demonstrate ischaemia, they are by no means the only changes of importance. Exercise induced ischaemia may occur in almost any lead and the common tendency to ignore changes in leads other than the lateral precordium should be discouraged.
ST Elevation in Leads without Q-Wave
ST elevation in leads without Q-waves can occur in few very different situations, both of which are fairly uncommon. The first is when patients have a very high grade proximal LAD stenosis or a high graft stenosis of a large right coronary artery. The ischaemia associated with ST depression is subendocardial whereas ischaemia producing ST elevation is transmural, affecting the full thickness of the heart. It follows that full thickness ischaemia is rare during exercise even with high grade proximal stenosis.The second cause of ST elevation is coronary spasm i.e. so severe that it completely obliterates antegrade flow through epicardial arteries. This has been termed Prinzmetals angina and is most commonly seen at rest, but very occasionally occurs with exercise. It is common for arrhythmias to accompany this process. It appears that patient with angiographically normal coronary arteries and Prinzmetal’s syndrome due to spasm usually have no change during exercise. If they have CAD, with or without spasm, ST elevation as well as depression may be seen. Exercise induced ST elevation in a subject with variant angina probably indicates hemodynamically significantn coronary atheroma.
The long term follow-up information suggests that patients whose ST depression evolves to downsloping have more severe disease than those that do not. Recently it has been reported that downsloping ST depression indicates that a larger area of myocardium is involved and that when the subepicardial muscle as well as the subendocardium is also ischaemic, is usually due to mutivessel disease. Downsloping pattern in V3 and V4 may be due to the additive effects of anterior wall subendocardial ischaemia superimposed on transmural posterior wall ischaemia.
Anterior transmural ischaemia results in ST elevation and would expect transmural posterior wall ischaemia would produce a vector in the same direction as the anterior subendocardial ischaemia process. Thus downsloping ST depression in V3 and V4 probably represents more severe ischaemia than horizontal. It may be a marker for multivessel disease.
ST Depression only on Recovery
Although ST depression during exercise often persists into recovery, it may not manifest until exercise has been terminated. The reasons for this are still not clear but the phenomena have been studied by several investigations. ST depression occurring in recovery only has the same significance as exercise induced ST changes.Time Course of ST Depression It has long been recognized that when ST depression comes on early at low workloads the degree of ischaemia is likely to be more severe. It has long been taught, when ST depression comes on at high workloads, but resolves very quickly after exercise, it constitutes a false positive ST depression. However, it has been found that significant CAD was more common than not, at least in those who were referred for angiography. As might be expected, patients with early onset, late offset ST depression usually had severe disease. Group of patients with resting ST depression increased with exercise, was found to have severe disease. It has often been stated that these patients should not be tested because the results would include a large number of false positives.This might be true if the patients are asymptomatic, but certainly does not pertain to those who have anginal chest pain. It must be cautioned that not all patients with rapid resolution of ST
depression during recovery have normal coronary arteries.
Magnitude of ST Depression
It is intuitive that the magnitude of ST depression should correlate with the degree of the ischaemia. In patients with left main or left main equivalent angiographic changes or with other severe degrees of the ischaemia, the magnitude of ST depression is greater. When 2 mm or more of ST depression is present the probability of left main disease increases. The degree of ST depression at higher workloads depends on what is used for the indication to terminate exercise.If patients are pushed enough, or if they have some degree of left ventricular hypertrophy they may have severe ST depression. If patients with single vessel disease are encouraged to exercise strenuously or if they have some degrees of LVH, they may have very severe ST depression.Bogaty found that in patients with 2 mm or more of ST depression, survival was determined by the duration of exercise on the Bruce protocol, not on the magnitude of depression. Thus the magnitude of ST depression at maximum workload, may not indicate the severity of coronary artery disease. Major ST depression at low workload indicates severe disease.
Distribution of ST Depression
Although it has been recognized for years that lead V4, V5 and V6 are most likely to demonstrate ischaemia, they are by no means the only changes of importance. Exercise induced ischaemia may occur in almost any lead and the common tendency to ignore changes in leads other than the lateral precordium should be discouraged.
ST Elevation in Leads without Q-Wave
ST elevation in leads without Q-waves can occur in few very different situations, both of which are fairly uncommon. The first is when patients have a very high grade proximal LAD stenosis or a high graft stenosis of a large right coronary artery. The ischaemia associated with ST depression is subendocardial whereas ischaemia producing ST elevation is transmural, affecting the full thickness of the heart. It follows that full thickness ischaemia is rare during exercise even with high grade proximal stenosis.The second cause of ST elevation is coronary spasm i.e. so severe that it completely obliterates antegrade flow through epicardial arteries. This has been termed Prinzmetals angina and is most commonly seen at rest, but very occasionally occurs with exercise. It is common for arrhythmias to accompany this process. It appears that patient with angiographically normal coronary arteries and Prinzmetal’s syndrome due to spasm usually have no change during exercise. If they have CAD, with or without spasm, ST elevation as well as depression may be seen. Exercise induced ST elevation in a subject with variant angina probably indicates hemodynamically significantn coronary atheroma.
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| ST Elevation in Leads with Q-Waves |
When ST elevation occurred during exercise in leads with Q-waves, it was originally believed that it was to a akinetic or dyskinetic segment. There seemed to be area of scar producing the ST elevation but it did not make sense that ST elevation which is experimentally clearly a current of injury, would come from scar tissue in the absence of injured calls. In recent reports, thallium scintigrams in areas of myocardium producing ST elevation suggest that there is usually on area of ischaemic muscle, usually adjacent to the scar. Thus, exercise, induced ST-segment elevation in areas of Q-waves probably identifies ischaemia and may also be a way of identifying hibernating myocardium Bertella reports that if QTC shortens 10 m/sec with exercise there is definitely viable myocardium.
ST Elevation at Rest (Early Repolarisation)
Although a stable LV aneurysm may manifest ST-segment elevation in the precordial leads at rest. Some subjects with normal hearts show a degree of elevation in the anterior precordial leads and also frontal leads. These phenomena, termed early repolarisation is most commonly seen in young black men but is by no means limited to this group (Grucins syndrome). It is found to be very common in well conditioned athletes. If this type of ST-segment elevation returns to normal during exercise, it is usually associated with a normal heart. When measuring for significant ST depression in these patients the resting ST level is not used as baseline, as in those with normal
ST-segments. Any exercise induced ST depression seen should be analyzed as if the resting ST were isoelectric. It has also been compared with the Brugada syndrome, where a similar pattern indicated the likelihood of severe, sometimes lethal arrhythmias.
Other Indices of ST Changes
Lead Strength (ST/R)
When the R-wave in the lateral precordial leads is less than 10 mm the sensitivity of ST depression is very low if 1 mm of ST depression is used as a standard. The corrected ST for R- wave amplitude is arrived at, by simply dividing the ST by the R-wave amplitude. When using 0.1 as a cut of for an abnormal test, the sensitivity is increased markedly, especially in those with R-waves less than 10 mm. When applying this method to patients with tall R-waves, the specificity is increased but as might be expected, the sensitivity is decreased. This type of correction should become standard practice in the future.
ST Heart Rate Slope
Correcting ST depression for heart rate, seems to be based on second physiological principles and has been proposed by a number of investigations. Elamin and associates reported that he could achieve 100 per cent sensitivity and specificity in the discrimination of CAD and could also separate with perfect accuracy one vessel, two vessel and three vessel disease. Unfortunately no one else has been able to confirm his findings. Kligfield et al have one extensive study using ST/HR slope and believe that it adds a good deal to the diagnostic accuracy. They use a slope of 2.4 micro volts/h/beat as a threshold for the presence of ischaemia (r = heart rate).
ST Heart Rate Index (Kligfield Index)
To calculate the index, the maximum ST depression is divided by the Delta heart rate (difference between the resting and maximum heart rate). As the calculation is very simple and not so dependent on a more gradual protocol, it has a considerable utility. It is important to remember that ST depression should be measured in fractions of a millimeter. When using an index of greater than 1.6 to identify ischaemia they report a sensitivity of 90 per cent and a specificity of 95 per cent.
ST Evolving Towards Normal with Exercise
Patients with abnormal autonomic drive have demonstrated ST-segment depression after hyperventilation as well as after exercise. Patients who display ST-segment depression at rest or an increased ST-segment depression after hyperventilation, in whom the depression tends to return to normal with exercise usually do not have epicardial CAD. Changes associated with hyperventilation are associated with normal coronary arteries. Propranolol and other beta- blockers have been shown to back the ST changes associated with hyperventilation, suggesting an autonomic etiology. The common findings that body position may produce similar changes tends to support this concept. These types of changes are common in patients with mitral prolapse.
Intermittent ST Depression
Several patients progress from variable ST-segment depression, often associated with respiration, to the classic ST-segment changes typical of ischaemia. The mechanism of this condition seems to be related to the fact that inspiration and expiration are associated with different rates of left ventricular filling. If the compliance of the left ventricle is slightly decreased the increased rates of the filling may produce an elevation in the end diastolic pressure and therefore, ST-segment depression for only a few beats. This is almost always seen near maximum stress levels, when compliance of the ventricle would be expected to be decreased the most and when the abdominal pump would be returning the blood to the heart at the greatest velocity.ST Depression with Long Diastolic Filling For the person with a slow heart rate and a long period of a diastole after a premature ventricular contraction, the next beat is often associated with ST-segment depression. It is well established that the individual has over filling of the ventricle and if the compliance is compromised, the increased diastolic pressure may be associated with ST-segment depression. This is seen repeatedly and correlates well with the diagnosis of clinical ischaemia. It is most commonly recorded after the exercise is terminated. This type of ST-segment depression has not been recognized in very young people with sinus arrhythmia or with heart block.
ST Hystersis (HR recovery ST loop)
The rate of recovery of ST depression has been recognized as a measure of ischaemia severity for many years. When comparing the magnitude of ST depression during recovery according to the time, with that just before termination of exercise, it has little discriminatory value. When recovery ST depression is plotted according to heart rate and composed to ST depression during exercise at similar heart rates, the results become more useful. A clockwise plot is common in normal patients who have ST depression, whereas, a counter clockwise plot depicts the ischaemic.
Rounded ST Depression
A rounded ST-segment depression pattern in the CM5 lead, as well as in the other leads, is common and is often associated with ischaemia. This pattern is somewhat difficult to evaluate if the duration of the ST-segment sagging is very short, but it usually reflects ventricular dysfunction. This pattern is associated with slightly increased incidence of subsequent coronary events. Patients with a rounded pattern had a 5.8 per cent per year incidence of coronary events,compared with 8.3 per cent per year for those with a horizontal pattern.
False Positive ST Changes
1) The slope of the PQ-segment can help predict the magnitude of the influence of P-wave depolarization and thus help predict which patient would have false positive ST- segments. This sign should be worked for in leads II and III and aVF and is most commonly seen when the P-wave amplitude is increased. It is believed that this is the reason that ST depression found only in these leads is more likely to be a false positive response.
2) Digitalis: It has long been recognized that digitalis may cause ST depression and that it is exaggerated by exercise.
3) Hypokalemia: There are many causes of hypokalemia that may induce ST depression in patients with normal coronary arteries.
4) Hyperventilation: Changes in T-wave with hyperventilation or standing are relatively common and are thought to be mediated through the autonomic nervous system. When they are associated with ST-segment depression the prevalence decreases, it has been reported to be less than 1 per cent to 2 per cent. The mechanism is somewhat obscure and has been attributed to pH changes, electrolyte changes (especially potassium), and changes in heart position, coronary arteriolar vasospasm and excessive catecholamines.
Because T-waves can be reduced by beta blockers and accentuated by intravenous epinephrine, the changes are probably mediated through the sympathetic pathway. When exercise induced ST-depression is found in patients who are likely to have non-coronary cause, it can be identified if the changes are abolished by a beta blocker. It has been found that the drug did not eliminate the ST depression in any patients with significant coronary artery disease, but did correct the ST in those with normal coronary angiogram.
ST Elevation at Rest (Early Repolarisation)
Although a stable LV aneurysm may manifest ST-segment elevation in the precordial leads at rest. Some subjects with normal hearts show a degree of elevation in the anterior precordial leads and also frontal leads. These phenomena, termed early repolarisation is most commonly seen in young black men but is by no means limited to this group (Grucins syndrome). It is found to be very common in well conditioned athletes. If this type of ST-segment elevation returns to normal during exercise, it is usually associated with a normal heart. When measuring for significant ST depression in these patients the resting ST level is not used as baseline, as in those with normal
ST-segments. Any exercise induced ST depression seen should be analyzed as if the resting ST were isoelectric. It has also been compared with the Brugada syndrome, where a similar pattern indicated the likelihood of severe, sometimes lethal arrhythmias.
Other Indices of ST Changes
Lead Strength (ST/R)
When the R-wave in the lateral precordial leads is less than 10 mm the sensitivity of ST depression is very low if 1 mm of ST depression is used as a standard. The corrected ST for R- wave amplitude is arrived at, by simply dividing the ST by the R-wave amplitude. When using 0.1 as a cut of for an abnormal test, the sensitivity is increased markedly, especially in those with R-waves less than 10 mm. When applying this method to patients with tall R-waves, the specificity is increased but as might be expected, the sensitivity is decreased. This type of correction should become standard practice in the future.
ST Heart Rate Slope
Correcting ST depression for heart rate, seems to be based on second physiological principles and has been proposed by a number of investigations. Elamin and associates reported that he could achieve 100 per cent sensitivity and specificity in the discrimination of CAD and could also separate with perfect accuracy one vessel, two vessel and three vessel disease. Unfortunately no one else has been able to confirm his findings. Kligfield et al have one extensive study using ST/HR slope and believe that it adds a good deal to the diagnostic accuracy. They use a slope of 2.4 micro volts/h/beat as a threshold for the presence of ischaemia (r = heart rate).
ST Heart Rate Index (Kligfield Index)
To calculate the index, the maximum ST depression is divided by the Delta heart rate (difference between the resting and maximum heart rate). As the calculation is very simple and not so dependent on a more gradual protocol, it has a considerable utility. It is important to remember that ST depression should be measured in fractions of a millimeter. When using an index of greater than 1.6 to identify ischaemia they report a sensitivity of 90 per cent and a specificity of 95 per cent.
ST Evolving Towards Normal with Exercise
Patients with abnormal autonomic drive have demonstrated ST-segment depression after hyperventilation as well as after exercise. Patients who display ST-segment depression at rest or an increased ST-segment depression after hyperventilation, in whom the depression tends to return to normal with exercise usually do not have epicardial CAD. Changes associated with hyperventilation are associated with normal coronary arteries. Propranolol and other beta- blockers have been shown to back the ST changes associated with hyperventilation, suggesting an autonomic etiology. The common findings that body position may produce similar changes tends to support this concept. These types of changes are common in patients with mitral prolapse.
Intermittent ST Depression
Several patients progress from variable ST-segment depression, often associated with respiration, to the classic ST-segment changes typical of ischaemia. The mechanism of this condition seems to be related to the fact that inspiration and expiration are associated with different rates of left ventricular filling. If the compliance of the left ventricle is slightly decreased the increased rates of the filling may produce an elevation in the end diastolic pressure and therefore, ST-segment depression for only a few beats. This is almost always seen near maximum stress levels, when compliance of the ventricle would be expected to be decreased the most and when the abdominal pump would be returning the blood to the heart at the greatest velocity.ST Depression with Long Diastolic Filling For the person with a slow heart rate and a long period of a diastole after a premature ventricular contraction, the next beat is often associated with ST-segment depression. It is well established that the individual has over filling of the ventricle and if the compliance is compromised, the increased diastolic pressure may be associated with ST-segment depression. This is seen repeatedly and correlates well with the diagnosis of clinical ischaemia. It is most commonly recorded after the exercise is terminated. This type of ST-segment depression has not been recognized in very young people with sinus arrhythmia or with heart block.
ST Hystersis (HR recovery ST loop)
The rate of recovery of ST depression has been recognized as a measure of ischaemia severity for many years. When comparing the magnitude of ST depression during recovery according to the time, with that just before termination of exercise, it has little discriminatory value. When recovery ST depression is plotted according to heart rate and composed to ST depression during exercise at similar heart rates, the results become more useful. A clockwise plot is common in normal patients who have ST depression, whereas, a counter clockwise plot depicts the ischaemic.
Rounded ST Depression
A rounded ST-segment depression pattern in the CM5 lead, as well as in the other leads, is common and is often associated with ischaemia. This pattern is somewhat difficult to evaluate if the duration of the ST-segment sagging is very short, but it usually reflects ventricular dysfunction. This pattern is associated with slightly increased incidence of subsequent coronary events. Patients with a rounded pattern had a 5.8 per cent per year incidence of coronary events,compared with 8.3 per cent per year for those with a horizontal pattern.
False Positive ST Changes
1) The slope of the PQ-segment can help predict the magnitude of the influence of P-wave depolarization and thus help predict which patient would have false positive ST- segments. This sign should be worked for in leads II and III and aVF and is most commonly seen when the P-wave amplitude is increased. It is believed that this is the reason that ST depression found only in these leads is more likely to be a false positive response.
2) Digitalis: It has long been recognized that digitalis may cause ST depression and that it is exaggerated by exercise.
3) Hypokalemia: There are many causes of hypokalemia that may induce ST depression in patients with normal coronary arteries.
4) Hyperventilation: Changes in T-wave with hyperventilation or standing are relatively common and are thought to be mediated through the autonomic nervous system. When they are associated with ST-segment depression the prevalence decreases, it has been reported to be less than 1 per cent to 2 per cent. The mechanism is somewhat obscure and has been attributed to pH changes, electrolyte changes (especially potassium), and changes in heart position, coronary arteriolar vasospasm and excessive catecholamines.
Because T-waves can be reduced by beta blockers and accentuated by intravenous epinephrine, the changes are probably mediated through the sympathetic pathway. When exercise induced ST-depression is found in patients who are likely to have non-coronary cause, it can be identified if the changes are abolished by a beta blocker. It has been found that the drug did not eliminate the ST depression in any patients with significant coronary artery disease, but did correct the ST in those with normal coronary angiogram.
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| False Positive ST Changes |
ST Depression in V1
Michaelides at al reported that 75 per cent of patients with these findings had right coronary disease with a sensitivity of 89 per cent. It seems likely that it is a rare but reliable marker for inferior wall ischaemia.
Localisation of Proximal or Distal LAD
When the narrowing is in the proximal LAD above the first diagonal, the following changes may be seen:
1) ST elevation in V1.
2) Decreased T-wave negativity in V1.
3) ST depression in two of the three leads II, III or aVF.
LAD below the Diagonal
The above triad is usually missing but ST depression is usually present in V4, V5, and V6.
Michaelides at al reported that 75 per cent of patients with these findings had right coronary disease with a sensitivity of 89 per cent. It seems likely that it is a rare but reliable marker for inferior wall ischaemia.
Localisation of Proximal or Distal LAD
When the narrowing is in the proximal LAD above the first diagonal, the following changes may be seen:
1) ST elevation in V1.
2) Decreased T-wave negativity in V1.
3) ST depression in two of the three leads II, III or aVF.
LAD below the Diagonal
The above triad is usually missing but ST depression is usually present in V4, V5, and V6.
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