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This table summarizes the findings of several investigations that compared the accuracy of CT angiography with standard quantitative coronary angiography.

Significant improvements were made with sixtyfour slice CT systems. How predictive then is noninvasive CT coronary angiography of coronary events?

A first investiga tion has only recently been published. Coronary angiography. Am J Radiol. They were followed for an average month period.

This reported high cardiac event rate is of concern because it seems to be inconsistent with that of other studies.

Yet, one of the reasons for this very high event rate is that the endpoints of the study included, in addition to death or nonfatal myocardial infarction, hospitalization for angina as well as revascularization.

The second reason for why the findings of this CT angiographic outcome study appear inconsistent with other findings is shown here.

On myocardial perfusion imaging, as shown by the green bar, a normal CT angiogram was highly accurate in ruling out the presence of functionally obstructive 8 Leber AW, Knez A, von Ziegler F, et al.

Symposium 19 7. Heinrich Schelbert coronary lesions because all stress myocardial perfusion images were normal.

Let us further compare the limited accuracy of CT angiography to that of PET stress-rest perfusion imaging for the detection of coronary disease.

An example of a rubidium PET study is shown here and shows an unequivocal stress perfusion defect. Here, the findings are made in 8 investigations including a total of patients are summarized.

They took advantage of a feature unique to PET that is acquisition of ECG gated perfusion images during peak stress, and calculated the change in left ventricular ejection fraction from rest to stress.

In regions with stress-induced defects however, subendocardial ischemia attenuates or abolishes this increase in contractile function.

The stress-related decline in the ejection fraction thus correctly identified the presence of extensive coronary artery disease.

This slide summarizes the findings of the Dorbala study. Another approach for identifying the extent of coronary artery disease entails measurements of myocardial blood flow and its response to vasodilator stress as is also now possible with PET.

Taken together, PET thus holds considerable promise for the accurate identification of coronary artery disease and for defining its extent and severity.

This question has recently been addressed by Merhige et al. The pre-test likelihood of coronary artery disease was similar for both patient groups.

It seems to me that one of the reasons for the lower postutilization of coronary angiography is, as other studies have reported, the higher interpretive confidence of PET, that is, the greater certainty that a given study is definitely normal or definitely abnormal, so that the lower number of equivocal perfusion imaging studies reduces the need for further diagnostic tests.

J Nuc Med. For example, the cardiac death rate is very low in individuals with normal perfusion images, but rises to 2.

This slide compares several parameters as described in a report by Iskandrian et al. Gender alone contains some predictive value.

The addition of coronary angiography raises the predictive value further but significantly increases when SPECT imaging is added.

The same is likely to apply also to PET, given its higher diagnostic performance. Importantly however, when coronary angiography is excluded, the predictive value remains high and does not decline.

Thus, it would appear that stress-rest perfusion imaging may assume a central role for predicting cardiac events and for risk stratification.

PET might become even more important in the future, given the recently published findings of the Courage Trial.

This trial found no difference in outcomes of patients with stable coronary artery disease who underwent optimum medical treatment when compared to a similar group again with optimum medical treatment but also with percutaneous coronary interventions.

Several speakers have already referred to imaging of the atherosclerotic plaque. Noninvasive approaches for imaging the atherosclerotic plaque have indeed attracted considerable interest.

This is because we now know that the majority of acute coronary events and myocardial infarctions result from rupture and erosion of atherosclerotic plaques.

N Engl J Med. F deoxyglucose PET images of the neck are compared to intravenous contrast CT angiographic images. The focally increased F deoxyglucose uptake in the right neck co-localizes on the fusion images with the angiographically visualized stenosis of the carotid artery on the CT images.

Histopathology and autoradiography with C labeled deoxyglucose of an atherosclerotic plaque, as seen on the next slide, shows the thin fibrous cap, the lipid core and numerous macrophages.

The C activity is seen to colocalize with macrophages, suggesting retention of F deoxyglucose in macrophages.

Studies by Tawakol et al. Tawakol et al. Based on available histopathologic data from patients with fatal myocardial infarctions, the carotid artery lesions were grouped by the fraction of macrophages in plaques.

When grouped in this way, F deoxyglucose concentrations were significantly higher in lesions considered vulnerable as compared to less vulnerable or stable lesions.

Symposium 21 7. Heinrich Schelbert in the coronary circulation will likely remain difficult and challenging, PET imaging of atherosclerotic plaques may offer an opportunity for assessing the effects of plaque stabilizing therapy.

In this example of a patient in the dietary group, extensive F deoxyglucose uptake is seen in both carotid arteries at baseline; no change is seen after 3 months.

This is different in the next example of a patient in the simvastatin treatment group, where the intense carotid artery F deoxyglucose uptake at baseline is no longer visualized at follow-up.

The next slide summarizes the findings in the 43 patients. The carotid artery F deoxyglucose uptake significantly declined in the simvastatin treatment group while no significant change occurred in the diet control group.

Effects of lipid lowering on vascular lesions have in fact been shown previously with MRI;19 however, significant changes were noted only after 12 months as compared to only 3 months in the PET study.

This then suggests that F deoxyglucose offers an opportunity for monitoring the efficacy of treatments intended to reduce vascular inflammation and to stabilize atherosclerotic plaques.

Is the noninvasive identification of early preclinical coronary atherosclerosis possible? The slide here illustrates the development and progression of coronary artery disease.

With progression of the disease, atherosclerotic plaques develop; the vessel lumen may remain fully preserved or be compromised only mildly.

Rupture or erosion of plaques leads to acute coronary events. The question I would like to address is whether we also can identify very early stages of the disease process, that is at a time before structural alterations have occurred and when the disease process is perhaps still reversible.

It may in fact be possible. With measurements of myocardial blood flow we can determine the responsiveness of the coronary circulation to adrenergic and pharmacologic vasodilator stimuli.

Myocardial blood flow can readily be measured with PET and radiotracers like O labeled water, rubidium or with N ammonia.

To determine whether functional alterations of the coronary circulation could in fact be demonstrated in apparently normal individuals yet with risk factors for coronary artery disease, we measured myocardial blood flow with N ammonia and PET at rest, then during adrenergic stimulation with cold pressor testing and again during pharmacologic vasodilation with dipyridamole.

When compared to a control group of individuals without risk factors for coronary artery disease, myocardial blood flow at rest and during dipyridamole stimulation were normal in the at-risk individuals.

However, the flow response to cold pressor testing was significantly diminished. With cold pressor testing, immersion of a hand in ice cold water prompts an immediate increase in heart rate and blood pressure, and consequently, in cardiac work.

It is associated in normal individuals with a proportionate flow increase. Attenuation of this normal flow response in the individuals at risk suggests that vasoconstrictor forces elicited by adrenergic stimulation are no longer adequately balanced by vasodilator forces, most likely because of a reduction in the nitric oxide bioavailability due to endothelial dysfunction.

This finding differed from those of other investigators who observed that risk factors did in fact impair the total vasodilator capacity.

We therefore asked whether conventional risk factors selectively targeted the endothelium or affected also the total integrated vascular function.

As Prior et al. This then suggests a possible association between the magnitude of the cardiac risk and the degree of functional compromise.

It may indeed initially be confined to the endothelium but subsequently encroaches upon the vascular smooth muscle. Yet, it remains uncertain whether this functional progression depends on the number of risk factors or on the degree of endothelial dysfunction alone or whether dysfunction of the endothelium and the vascular smooth muscle occur in parallel.

It also remains uncertain whether such progressive vascular dysfunction is related to the duration of the disease with a possible development of structural alterations.

It seems to me that there may indeed be a clinical or practical role for measurements of coronary responsiveness. One is the assessment of cardiac risk, a second one the assessment of risk modification strategies and, finally, the possibility of assessing the efficacy of novel vasoactive drugs.

If in fact an abnormal responsiveness of the coronary circulation reflects endothelial dysfunction, then it should contain predictive information.

This in fact has been demonstrated by Schindler et al. Ann Intern Med. Administration of Valsartan for 12 weeks in individuals with impaired glucose tolerance was associated with restoration of the flow response to cold that however reverted to the abnormal baseline state after Valsartan had been discontinued for 3 months.

An important question is whether such drug mediated restoration of endothelial function would improve the long term outlook of at risk patients.

Direct evidence is still missing but findings made in a study that assessed endothelial function of the brachial artery might suggest so.

On brachial artery flow measurements at baseline, the flow-mediated diameter increase as a measure of endothelial function was diminished in all women.

After 6 months of aggressive antihypertensive treatment, forearm blood flow measurements were repeated. This then suggests that therapeutic targeting of endothelial dysfunction may in fact translate into long term benefits.

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In the United States, this new and exciting technology has really caught on. So the question is: What will be the clinical value of noninvasive CTangiography and what will be its impact on patient diagnosis and risk stratification?

This table summarizes the findings of several investigations that compared the accuracy of CT angiography with standard quantitative coronary angiography.

Significant improvements were made with sixtyfour slice CT systems. How predictive then is noninvasive CT coronary angiography of coronary events?

A first investiga tion has only recently been published. Coronary angiography. Am J Radiol. They were followed for an average month period.

This reported high cardiac event rate is of concern because it seems to be inconsistent with that of other studies.

Yet, one of the reasons for this very high event rate is that the endpoints of the study included, in addition to death or nonfatal myocardial infarction, hospitalization for angina as well as revascularization.

The second reason for why the findings of this CT angiographic outcome study appear inconsistent with other findings is shown here.

On myocardial perfusion imaging, as shown by the green bar, a normal CT angiogram was highly accurate in ruling out the presence of functionally obstructive 8 Leber AW, Knez A, von Ziegler F, et al.

Symposium 19 7. Heinrich Schelbert coronary lesions because all stress myocardial perfusion images were normal. Let us further compare the limited accuracy of CT angiography to that of PET stress-rest perfusion imaging for the detection of coronary disease.

An example of a rubidium PET study is shown here and shows an unequivocal stress perfusion defect. Here, the findings are made in 8 investigations including a total of patients are summarized.

They took advantage of a feature unique to PET that is acquisition of ECG gated perfusion images during peak stress, and calculated the change in left ventricular ejection fraction from rest to stress.

In regions with stress-induced defects however, subendocardial ischemia attenuates or abolishes this increase in contractile function.

The stress-related decline in the ejection fraction thus correctly identified the presence of extensive coronary artery disease.

This slide summarizes the findings of the Dorbala study. Another approach for identifying the extent of coronary artery disease entails measurements of myocardial blood flow and its response to vasodilator stress as is also now possible with PET.

Taken together, PET thus holds considerable promise for the accurate identification of coronary artery disease and for defining its extent and severity.

This question has recently been addressed by Merhige et al. The pre-test likelihood of coronary artery disease was similar for both patient groups.

It seems to me that one of the reasons for the lower postutilization of coronary angiography is, as other studies have reported, the higher interpretive confidence of PET, that is, the greater certainty that a given study is definitely normal or definitely abnormal, so that the lower number of equivocal perfusion imaging studies reduces the need for further diagnostic tests.

J Nuc Med. For example, the cardiac death rate is very low in individuals with normal perfusion images, but rises to 2.

This slide compares several parameters as described in a report by Iskandrian et al. Gender alone contains some predictive value.

The addition of coronary angiography raises the predictive value further but significantly increases when SPECT imaging is added. The same is likely to apply also to PET, given its higher diagnostic performance.

Importantly however, when coronary angiography is excluded, the predictive value remains high and does not decline.

Thus, it would appear that stress-rest perfusion imaging may assume a central role for predicting cardiac events and for risk stratification.

PET might become even more important in the future, given the recently published findings of the Courage Trial. This trial found no difference in outcomes of patients with stable coronary artery disease who underwent optimum medical treatment when compared to a similar group again with optimum medical treatment but also with percutaneous coronary interventions.

Several speakers have already referred to imaging of the atherosclerotic plaque. Noninvasive approaches for imaging the atherosclerotic plaque have indeed attracted considerable interest.

This is because we now know that the majority of acute coronary events and myocardial infarctions result from rupture and erosion of atherosclerotic plaques.

N Engl J Med. F deoxyglucose PET images of the neck are compared to intravenous contrast CT angiographic images.

The focally increased F deoxyglucose uptake in the right neck co-localizes on the fusion images with the angiographically visualized stenosis of the carotid artery on the CT images.

Histopathology and autoradiography with C labeled deoxyglucose of an atherosclerotic plaque, as seen on the next slide, shows the thin fibrous cap, the lipid core and numerous macrophages.

The C activity is seen to colocalize with macrophages, suggesting retention of F deoxyglucose in macrophages. Studies by Tawakol et al.

Tawakol et al. Based on available histopathologic data from patients with fatal myocardial infarctions, the carotid artery lesions were grouped by the fraction of macrophages in plaques.

When grouped in this way, F deoxyglucose concentrations were significantly higher in lesions considered vulnerable as compared to less vulnerable or stable lesions.

Symposium 21 7. Heinrich Schelbert in the coronary circulation will likely remain difficult and challenging, PET imaging of atherosclerotic plaques may offer an opportunity for assessing the effects of plaque stabilizing therapy.

In this example of a patient in the dietary group, extensive F deoxyglucose uptake is seen in both carotid arteries at baseline; no change is seen after 3 months.

This is different in the next example of a patient in the simvastatin treatment group, where the intense carotid artery F deoxyglucose uptake at baseline is no longer visualized at follow-up.

The next slide summarizes the findings in the 43 patients. The carotid artery F deoxyglucose uptake significantly declined in the simvastatin treatment group while no significant change occurred in the diet control group.

Effects of lipid lowering on vascular lesions have in fact been shown previously with MRI;19 however, significant changes were noted only after 12 months as compared to only 3 months in the PET study.

This then suggests that F deoxyglucose offers an opportunity for monitoring the efficacy of treatments intended to reduce vascular inflammation and to stabilize atherosclerotic plaques.

Is the noninvasive identification of early preclinical coronary atherosclerosis possible? The slide here illustrates the development and progression of coronary artery disease.

With progression of the disease, atherosclerotic plaques develop; the vessel lumen may remain fully preserved or be compromised only mildly.

Rupture or erosion of plaques leads to acute coronary events. The question I would like to address is whether we also can identify very early stages of the disease process, that is at a time before structural alterations have occurred and when the disease process is perhaps still reversible.

It may in fact be possible. With measurements of myocardial blood flow we can determine the responsiveness of the coronary circulation to adrenergic and pharmacologic vasodilator stimuli.

Myocardial blood flow can readily be measured with PET and radiotracers like O labeled water, rubidium or with N ammonia.

To determine whether functional alterations of the coronary circulation could in fact be demonstrated in apparently normal individuals yet with risk factors for coronary artery disease, we measured myocardial blood flow with N ammonia and PET at rest, then during adrenergic stimulation with cold pressor testing and again during pharmacologic vasodilation with dipyridamole.

When compared to a control group of individuals without risk factors for coronary artery disease, myocardial blood flow at rest and during dipyridamole stimulation were normal in the at-risk individuals.

However, the flow response to cold pressor testing was significantly diminished. With cold pressor testing, immersion of a hand in ice cold water prompts an immediate increase in heart rate and blood pressure, and consequently, in cardiac work.

It is associated in normal individuals with a proportionate flow increase. Attenuation of this normal flow response in the individuals at risk suggests that vasoconstrictor forces elicited by adrenergic stimulation are no longer adequately balanced by vasodilator forces, most likely because of a reduction in the nitric oxide bioavailability due to endothelial dysfunction.

This finding differed from those of other investigators who observed that risk factors did in fact impair the total vasodilator capacity.

We therefore asked whether conventional risk factors selectively targeted the endothelium or affected also the total integrated vascular function.

As Prior et al. This then suggests a possible association between the magnitude of the cardiac risk and the degree of functional compromise.

It may indeed initially be confined to the endothelium but subsequently encroaches upon the vascular smooth muscle.

Yet, it remains uncertain whether this functional progression depends on the number of risk factors or on the degree of endothelial dysfunction alone or whether dysfunction of the endothelium and the vascular smooth muscle occur in parallel.

It also remains uncertain whether such progressive vascular dysfunction is related to the duration of the disease with a possible development of structural alterations.

It seems to me that there may indeed be a clinical or practical role for measurements of coronary responsiveness. One is the assessment of cardiac risk, a second one the assessment of risk modification strategies and, finally, the possibility of assessing the efficacy of novel vasoactive drugs.

If in fact an abnormal responsiveness of the coronary circulation reflects endothelial dysfunction, then it should contain predictive information.

This in fact has been demonstrated by Schindler et al. Ann Intern Med. Administration of Valsartan for 12 weeks in individuals with impaired glucose tolerance was associated with restoration of the flow response to cold that however reverted to the abnormal baseline state after Valsartan had been discontinued for 3 months.

An important question is whether such drug mediated restoration of endothelial function would improve the long term outlook of at risk patients.

Direct evidence is still missing but findings made in a study that assessed endothelial function of the brachial artery might suggest so.

On brachial artery flow measurements at baseline, the flow-mediated diameter increase as a measure of endothelial function was diminished in all women.

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3 Comments

  1. Memi Dushakar

    Ich entschuldige mich, aber mir ist ganz anderes notwendig. Wer noch, was vorsagen kann?

  2. Fenrijin Yozshugrel

    Ich denke, dass Sie nicht recht sind. Geben Sie wir werden es besprechen.

  3. Nikojas Doujar

    Nicht so kommt es)))) vor

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