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Findings from my Stress and Nuclear test
Hello
I recently went for my regular Stress and Nuclear tests. The results from my Stress test is as follows:
Stress test conclusion: Good exercise tolerance, No chest pain, EKG negative for ischemia, No Arrhythmias, No ST-T changes, Pre-test BP - 100/70 and Post test 150/60, Normal Sinus rhythm
Nuclear test results: Small, questionable area of mild, partially reversible defect involving the anterior wall, Normal LV function with EF at 64%
My cardio suggests going for an angiogram. I am very concerned going for a Cath. I am 38 years old with a history of high cholesterol. (under control for the last 6 - 7 years; On Lipitor 10 Mg)
Could you please suggest based on your experiences? Is it advisable to go for a Cath now or wait and do a repeat stress/Nuclear test say after 6 months?
Is this a difficult condition? I am concerned and please help me with your inputs.
Regards
Murugan
I recently went for my regular Stress and Nuclear tests. The results from my Stress test is as follows:
Stress test conclusion: Good exercise tolerance, No chest pain, EKG negative for ischemia, No Arrhythmias, No ST-T changes, Pre-test BP - 100/70 and Post test 150/60, Normal Sinus rhythm
Nuclear test results: Small, questionable area of mild, partially reversible defect involving the anterior wall, Normal LV function with EF at 64%
My cardio suggests going for an angiogram. I am very concerned going for a Cath. I am 38 years old with a history of high cholesterol. (under control for the last 6 - 7 years; On Lipitor 10 Mg)
Could you please suggest based on your experiences? Is it advisable to go for a Cath now or wait and do a repeat stress/Nuclear test say after 6 months?
Is this a difficult condition? I am concerned and please help me with your inputs.
Regards
Murugan
QUOTE:
________________________________________________________________
I had an angiogram and was told my arteries were clear. No mention of all this you guys are talking about here. What qualifies someone for IVUS? What signs may show that someone has "vulnerable plaque"...high BP, high cholesterol? Thanks for your information! I'm thinking I don't need to worry too much yet, I'm only 34, but don't want anymore heart problems. Any advice on preventing the plaque from building up?
____________________________________________________________________
There are two different issues associated with plaque: The hard calcified plaque an easily identified formation during an angioplasty and treated to open a blocked vessel, and the vulnerable soft plaque that easily ruptures, forms a clot and is responsible for an acute heart attack.
In addition to sharing morphological characteristics of the plaque itself, the occurrence of disruption seems to become a more likely clinical event in patients who share some common systemic signs, including high serum total cholesterol, a high total cholesterol to high-density lipoprotein cholesterol ratio, and elevated levels of C-reactive protein (CRP). Such associations have prompted the notion of a "vulnerable patient"who is likely to have more than one vulnerable lesion. For many of these systemic characteristics, it still remains unclear if they are the cause or the effect of lesion vulnerability. A similar question continues to apply to any of the newly proposed systemic or local factors that have been associated with plaque instability, including the matrix metalloproteinases (MMPs).
The notion of "vulnerable atherosclerotic plaque" introduced many years ago has been since used frequently and liberally. VAP is a phrase to refer to intact lesions that look similar to those previously found to be disrupted and complicated by thrombosis on pathological examination. In doing so, it was assumed that given enough time or the right stimulus, these would become disrupted, thus triggering the formation of a thrombus.
Patients dying from acute myocardial infarction are usually associated with <50% diameter stenosis, explaining the relatively recent realization of the danger these plaques may harbor. Other overall characteristics commonly associated with ruptured plaques include their propensity to have an eccentrically located lumen, as well as the significantly enhanced compensatory enlargement of the affected segment. AHA, AAC guidelines recommends stents for 70% or greater occlusions and generally no consideration to less than 50% occlusions.
Atherosclerosis and its consequences are the most rapidly growing vascular pathology in both developing and developed countries. However, most atherosclerotic plaques will remain harmless and only vulnerable plaques (a minority) have the potential of causing myocardial infarction. Disruption of the vulnerable plaque or plaque erosion and subsequent thrombosis (clots) is the most common pathophysiological mechanism leading to an acute coronary syndrome.
Given the clinical importance of coronary plaque rupture and its consequences, a growing interest exists in the development and improvement of diagnostic modalities that will promptly and most importantly accurately detect and characterize the high-risk atheromatous plaque. These techniques may help risk stratification and allow the selection of the most appropriate therapeutic approaches. Current available techniques can be separated into invasive and non-invasive, the former providing more accurate information at this point of time, but non-invasive techniques are quite promising but require future follow up studies.
Cardiovascular disease continues to be the leading cause of death and disability in the developed world. The causes of most heart attacks and strokes are vulnerable coronary and carotid plaques that are not detectable by current diagnostic methods. It is generally thought that the most common histologic type of vulnerable plaque is a lesion with a thin fibrous cap, a large lipid pool, and abundant macrophages. If such plaques could be detected and treated prior to disruption, a major advance in healthcare would be achieved
Description is non-vulnerable plaque with fibrous tissue that partially blocks blood flow but not likely to cause a clot or cardiac event....vulnerable plaque with a lipid-rich core and a thin fibrous cap. Explanation the large, calcified plaque growing on the inside surface of coronary arteries is not the cause of most heart attacks. Rather, the primary culprit is the soft, relatively small "vulnerable" plaque that forms within the vessel walls and identified by IVUS.
Large, calcified plaque is actually relatively stable and, because of its hard calcified covering, less commonly cracks. The more dynamic, less stable soft plaque is much more likely to suddenly rupture. As the body forms a clot to try to heal such a rupture, the result may be a total blockage of blood flow; in other words, a heart attack. The soft plaque is hidden inside the walls of the artery and often causes no obvious blockage or loss of blood flow until, of course, the often-fatal rupture.
Yet there is good news hidden in this new understanding because the buildup of soft, vulnerable plaque is much easier to reverse than that of hard, calcified plaque (I have no source for reversal). Levels of the two types of plaque are related, since the same process appears to result in both forms. One prevalent theory on the origin of the hard plaque is that it's the body's attempt to protect the artery from vulnerable plaque by covering it with a hard, calcified layer. However, bypass surgery and balloon angioplasty do not slow down the process of soft or hard plaque formation; they often accelerate them.
Some history: An early research study in 1986 by Dr. Greg Brown of the University of Washington at Seattle demonstrated that sudden blockages causing heart attacks were occurring in locations of coronary arteries that had very little plaque, not nearly enough to qualify for bypass or angioplasty surgery. In the late 1980s, Dr. Steven Nissen of the Cleveland Clinic began to examine the coronary arteries of heart patients with an innovative ultrasound camera that he guided into the blood vessels. He found many soft bulges of plaque, often numbering into the hundreds in a single patient, but relatively few areas of calcified plaque. He proposed the idea that it was these widely distributed soft bulges of plaque, not the deposits of hard plaque, that were the primary culprit behind heart attacks. Brown's and Nissen's research, as well as similar studies, were slow to be accepted. Recently, Dr. Nissen has emerged as a leading innovator in fostering new therapies for heart disease, playing a leading role in several new drugs. Dr. Nissen also conducted an important study that indicates that lowering LDL cholesterol to levels significantly below the standard recommendations reduces risk.
________________________________________________________________
I had an angiogram and was told my arteries were clear. No mention of all this you guys are talking about here. What qualifies someone for IVUS? What signs may show that someone has "vulnerable plaque"...high BP, high cholesterol? Thanks for your information! I'm thinking I don't need to worry too much yet, I'm only 34, but don't want anymore heart problems. Any advice on preventing the plaque from building up?
____________________________________________________________________
There are two different issues associated with plaque: The hard calcified plaque an easily identified formation during an angioplasty and treated to open a blocked vessel, and the vulnerable soft plaque that easily ruptures, forms a clot and is responsible for an acute heart attack.
In addition to sharing morphological characteristics of the plaque itself, the occurrence of disruption seems to become a more likely clinical event in patients who share some common systemic signs, including high serum total cholesterol, a high total cholesterol to high-density lipoprotein cholesterol ratio, and elevated levels of C-reactive protein (CRP). Such associations have prompted the notion of a "vulnerable patient"who is likely to have more than one vulnerable lesion. For many of these systemic characteristics, it still remains unclear if they are the cause or the effect of lesion vulnerability. A similar question continues to apply to any of the newly proposed systemic or local factors that have been associated with plaque instability, including the matrix metalloproteinases (MMPs).
The notion of "vulnerable atherosclerotic plaque" introduced many years ago has been since used frequently and liberally. VAP is a phrase to refer to intact lesions that look similar to those previously found to be disrupted and complicated by thrombosis on pathological examination. In doing so, it was assumed that given enough time or the right stimulus, these would become disrupted, thus triggering the formation of a thrombus.
Patients dying from acute myocardial infarction are usually associated with <50% diameter stenosis, explaining the relatively recent realization of the danger these plaques may harbor. Other overall characteristics commonly associated with ruptured plaques include their propensity to have an eccentrically located lumen, as well as the significantly enhanced compensatory enlargement of the affected segment. AHA, AAC guidelines recommends stents for 70% or greater occlusions and generally no consideration to less than 50% occlusions.
Atherosclerosis and its consequences are the most rapidly growing vascular pathology in both developing and developed countries. However, most atherosclerotic plaques will remain harmless and only vulnerable plaques (a minority) have the potential of causing myocardial infarction. Disruption of the vulnerable plaque or plaque erosion and subsequent thrombosis (clots) is the most common pathophysiological mechanism leading to an acute coronary syndrome.
Given the clinical importance of coronary plaque rupture and its consequences, a growing interest exists in the development and improvement of diagnostic modalities that will promptly and most importantly accurately detect and characterize the high-risk atheromatous plaque. These techniques may help risk stratification and allow the selection of the most appropriate therapeutic approaches. Current available techniques can be separated into invasive and non-invasive, the former providing more accurate information at this point of time, but non-invasive techniques are quite promising but require future follow up studies.
Cardiovascular disease continues to be the leading cause of death and disability in the developed world. The causes of most heart attacks and strokes are vulnerable coronary and carotid plaques that are not detectable by current diagnostic methods. It is generally thought that the most common histologic type of vulnerable plaque is a lesion with a thin fibrous cap, a large lipid pool, and abundant macrophages. If such plaques could be detected and treated prior to disruption, a major advance in healthcare would be achieved
Description is non-vulnerable plaque with fibrous tissue that partially blocks blood flow but not likely to cause a clot or cardiac event....vulnerable plaque with a lipid-rich core and a thin fibrous cap. Explanation the large, calcified plaque growing on the inside surface of coronary arteries is not the cause of most heart attacks. Rather, the primary culprit is the soft, relatively small "vulnerable" plaque that forms within the vessel walls and identified by IVUS.
Large, calcified plaque is actually relatively stable and, because of its hard calcified covering, less commonly cracks. The more dynamic, less stable soft plaque is much more likely to suddenly rupture. As the body forms a clot to try to heal such a rupture, the result may be a total blockage of blood flow; in other words, a heart attack. The soft plaque is hidden inside the walls of the artery and often causes no obvious blockage or loss of blood flow until, of course, the often-fatal rupture.
Yet there is good news hidden in this new understanding because the buildup of soft, vulnerable plaque is much easier to reverse than that of hard, calcified plaque (I have no source for reversal). Levels of the two types of plaque are related, since the same process appears to result in both forms. One prevalent theory on the origin of the hard plaque is that it's the body's attempt to protect the artery from vulnerable plaque by covering it with a hard, calcified layer. However, bypass surgery and balloon angioplasty do not slow down the process of soft or hard plaque formation; they often accelerate them.
Some history: An early research study in 1986 by Dr. Greg Brown of the University of Washington at Seattle demonstrated that sudden blockages causing heart attacks were occurring in locations of coronary arteries that had very little plaque, not nearly enough to qualify for bypass or angioplasty surgery. In the late 1980s, Dr. Steven Nissen of the Cleveland Clinic began to examine the coronary arteries of heart patients with an innovative ultrasound camera that he guided into the blood vessels. He found many soft bulges of plaque, often numbering into the hundreds in a single patient, but relatively few areas of calcified plaque. He proposed the idea that it was these widely distributed soft bulges of plaque, not the deposits of hard plaque, that were the primary culprit behind heart attacks. Brown's and Nissen's research, as well as similar studies, were slow to be accepted. Recently, Dr. Nissen has emerged as a leading innovator in fostering new therapies for heart disease, playing a leading role in several new drugs. Dr. Nissen also conducted an important study that indicates that lowering LDL cholesterol to levels significantly below the standard recommendations reduces risk.
I had the same results, but again a clean angiogram does not mean you are out of the woods yet. Watch "The hidden epidemic" on PBS.org. It explains a lot. How to prevent plaque ? That's the billion dollar question even scientists are having a hard time with. Buy a good book on heart disease and you will have much better knowledgeon the subject.
How do you guys know so much about this? Are you in the medical profession or just read a lot or do you have doctors who explain all of this to you. I had an angiogram and was told my arteries were clear. No mention of all this you guys are talking about here. What qualifies someone for IVUS? What signs may show that someone has "vulnerable plaque"...high BP, high cholesterol? Thanks for your information! I'm thinking I don't need to worry too much yet, I'm only 34, but don't want anymore heart problems. Any advice on preventing the plaque from building up?
Your arteries first try to remodel themselves outward with plaque and normally only close in (stenosis) when the disease process (atherosclerosis) is advanced. That means you can have a considerable amount of plaque without it showing on an angiogram.
IVUS has an ultrasound transmitter attached to a cath. The ultra sound enables the recording and sending images to a monitor. The images are a cross section of the anatomy of the vessel and it shows plague within the artery wall that is missed by an angiogram.
In the early 1990s, IVUS research on the re-stenosis problem after angioplasty lead to recognition that most of the re-stenosis problem (as visualized by an angiography examination) was not true re-stenosis.
Perhaps the greatest contribution to understanding, so far, was achieved by clinical research trials completed in the United States in the late 1990s, using combined angiography and IVUS examination, to study which coronary lesions most commonly result in a myocardial infarction.
The studies revealed that most myocardial infarctions occur at areas with extensive atheroma within the artery wall, however very little stenosis of the artery opening. The range of lumen stenosis locations at which myocardial infarctions occurred ranged from areas of mild dilatation all the way to areas of greater than 95% stenosis. However the average or typical stenosis at which myocardial infarctions occurred were found to be less than 50%, describing plaques long considered insignificant by many. Only 14% of heart attacks occurred at locations with 75% or more stenosis, the severe stenoses previously thought by many to present the greatest danger to the individual. This research has changed the primary focus for heart attack prevention from severe narrowing to vulnerable plaque.
In the early 1990s, IVUS research on the re-stenosis problem after angioplasty lead to recognition that most of the re-stenosis problem (as visualized by an angiography examination) was not true re-stenosis.
Perhaps the greatest contribution to understanding, so far, was achieved by clinical research trials completed in the United States in the late 1990s, using combined angiography and IVUS examination, to study which coronary lesions most commonly result in a myocardial infarction.
The studies revealed that most myocardial infarctions occur at areas with extensive atheroma within the artery wall, however very little stenosis of the artery opening. The range of lumen stenosis locations at which myocardial infarctions occurred ranged from areas of mild dilatation all the way to areas of greater than 95% stenosis. However the average or typical stenosis at which myocardial infarctions occurred were found to be less than 50%, describing plaques long considered insignificant by many. Only 14% of heart attacks occurred at locations with 75% or more stenosis, the severe stenoses previously thought by many to present the greatest danger to the individual. This research has changed the primary focus for heart attack prevention from severe narrowing to vulnerable plaque.
Can you explain more about a regular angiogram not showing "disease?" This is the first I've heard this. Where does this information come from?
Thanks
Thanks
The primary disadvantages of IVUS being used routinely in a cardiac catheterization laboratory are its expense, the increase in the time of the procedure, and the fact that it is considered an interventional procedure, and should only be performed by angiographers that are trained in interventional cardiology techniques. In addition, there may be additional risk imposed by the use of the IVUS catheter.
While not a routinely used device -- like all catheter-based procedures, it is invasive, and there are costs associated with it -- in certain situations, IVUS can aid in the selection and sizing of stents and balloons, and can offer assurance that a stent has been properly deployed. This is of increasing importance in the era of drug-eluting stents. Research conducted using IVUS has also shown that one of the causes of restenosis may be inadequate dilatation -- that physicians, concerned with injuring or dissecting the artery itself, have tended to undersize the balloons. (See "Intravascular Ultrasound May Help Prevent Late Stent Thrombosis")
While not a routinely used device -- like all catheter-based procedures, it is invasive, and there are costs associated with it -- in certain situations, IVUS can aid in the selection and sizing of stents and balloons, and can offer assurance that a stent has been properly deployed. This is of increasing importance in the era of drug-eluting stents. Research conducted using IVUS has also shown that one of the causes of restenosis may be inadequate dilatation -- that physicians, concerned with injuring or dissecting the artery itself, have tended to undersize the balloons. (See "Intravascular Ultrasound May Help Prevent Late Stent Thrombosis")
I would not do an angiogram unless it is an IVUS version. Thats intra vascular ultrasound. A regular angiogram does not show soft plaque unless you already have blockage. You can pass a normal angiogram and still have lots of disease.
Why did you have the stress echo and nuclear tests to begin with? High Cholesterol? If there is some concern you have coronary artery disease AND you have this minor impaired wall movement, a cath might be a good idea. How adament is your cardiologist that you have the cath? Remember, Tim Russert (who I know some are sick of discussing) died of a heart attack brought on by asymptomatic coronary artery disease. I'm wondering what might be if he had had a cardiac cath. Maybe he did, I don't know.
Another thing to consider, if you're worried about your heart, the cardiac cath may help put your mind at rest.
Another thing to consider, if you're worried about your heart, the cardiac cath may help put your mind at rest.
It wouldn't be difficult for me to make a decision, I would not have an interventional procedure unless I was experiencing uncontrolled angina, shortness of breath, or unexplained fatigue.
Your EF is well within the normal range, and if there is any impaired wall movement, it is minor and almost insignificant. You don't appear to have any vessel occlusion, your choles is good so it may be safe to say you don't have an ischemic heart problem. If the wall impairment is due to heart muscle disease, then a cath to take a biopsy be considered!
Your EF is well within the normal range, and if there is any impaired wall movement, it is minor and almost insignificant. You don't appear to have any vessel occlusion, your choles is good so it may be safe to say you don't have an ischemic heart problem. If the wall impairment is due to heart muscle disease, then a cath to take a biopsy be considered!
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