EBCT does not meet "principles of screening" and cannot be advocated in asymptomatic people
Boston, MA - Electron-beam computer tomography (EBCT) cannot be advocated in people with no symptoms of heart disease, according to a Commentary in the December 14, 2005 issue of the Journal of the American Medical Association [1]. Using five established principles for defining an effective screening test, Dr Dariush Mozaffarian (Brigham and Women's Hospital, Boston, MA) concludes that large, long-term clinical trials are needed before EBCT can be used to predict cardiovascular risk in asymptomatic individuals.
Experts have debated the utility of EBCT as a risk-prediction tool ever since the technology first became widely available, with much of the controversy stemming from the fact that the test has been aggressively marketed to consumers. To heartwire, Mozaffarian acknowledged that disagreement over the value of EBCT is by no means new, but the issue has not been approached from the perspective he took in his Commentary.
"I did not think the debate had been framed in terms of fundamental principles of screening, which are essential to consider in determining the role of EBCT for screening," he explained to heartwire.
Principles of screening
According to his JAMA Commentary, these principlesare that the test screen for a disease that is common, serious, and at a preclinical stage such that preventive steps are possible. The test must also have the ability to distinguish between people who are likely or unlikely to develop disease; it must detect a disease that can be treated such that mortality and morbidity are reduced; it must be safe, cost-effective, and widely available; and it must be "ethically justifiable" after intended and unintended consequences of positive or negative results are taken into account.
As such, writes Mozaffarian, coronary heart disease (CHD) is indisputably an "attractive target" for screening since it is common, with an extended preclinical phase. Six studies, he notes, have addressed the question of whether EBCT can predict future events in asymptomatic patients, and all showed that people with the most abnormal coronary calcium scores were more likely to have cardiac events; however, the majority of people with an abnormal test result did not experience clinical events during follow-up, ranging from one to six years. Even more striking is Mozaffarian's observation that EBCT studies have not reported effects of testing on hard clinical outcomes, like MI and death. Added to this is the fact that the test entails radiation exposure, is not cheap (approximately $500 US), and is not widely available in rural areas or outside the US.
"Before EBCT screening for CHD in asymptomatic individuals can be justified, there must be evidence that benefits outweigh risks, and this evidence is currently lacking," Mozaffarian emphasized to heartwire. "Randomized trials are needed to provide this evidence."
Finally, addressing whether EBCT is ethical, Mozaffarian points out that false-positive test results can lead to additional unnecessary treatments that add additional cost and risk. Likewise, negative test results could have the unintended consequence of reducing an individual's commitment to a healthy lifestyle and other preventive strategies.
"Most people with a 'positive' EBCT screen will not suffer an event in the ensuing four to six years, and it is unclear how a positive EBCT screen would alter most preventive treatments received in the absence of screening," Mozaffarian explained to heartwire. "Randomized controlled trials are needed to determine whether EBCT screening for CHD in asymptomatic individuals results in net benefit, harm, or no effect."
Source
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Mozaffarian D. Electron-beam computed tomography for coronary calcium. JAMA 2005; 294:2897 -2901.
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December 24, 2005 01:13 (EST)
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Its hard to know where to begin---Mozaffarian is totally ignorant
It continues to amaze those of us with any experience using EBCT imaging for risk stratification to continue to witness individuals with zero experience in the field publish this nonsense---JAMA has a history of accepting such shoddy work as Mozaffarian's.
It is hard to know where to begin. An EBT calcium score is 10 times more predictive than any risk factor or a CRP---and he argues that most patients do not get an event in the next few years?---a ridiculous statement. Does he actually know the radiation dose? And there are NO false positives, doctor!!---By the way, a test with a 98% negative predictive value for stenosis is used by the experts to limit unnecessary followup exams---not lead to further testing!!
Has this doctor reviewed any of the data showing how poorly framingham performs compared to a calcium score?
Depressing work, Mozaffarian!!! |
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December 24, 2005 06:05 (EST)
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It's relative..........
James,
I'd like to interject the following thought. The statement that "there are no false positives" is relative.
A 75 year old with a calcium score of 400 may not necessarily have high grade fixed obstruction or large territories of reversible ischemia. Therefore, for the older age group, this finding begats cath work that might be avoided if stress testing were undertaken first. On the other hand, a 75 year old with a negative calcium score can be fairly reassured that significant obstructing coronary disease is not present.
So, the term false positive is really a true positive with regard to endothelial pathology, but not necessarily a true positive for significant reversible ischemia. It's relative to what you choose to reference.
Melissa |
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December 24, 2005 10:12 (EST)
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false negatives - two (or more) types of plaque
Melissa and James, calcified plaque in many cases may represent older arterial disease or plaque that may be related to non-traditional risk factors such as infectious origins. It is my experience that frequently low risk individuals may have high calcium scores and visa versa. There is ample literature relating periodontal diease with 2-3 x increased risk for CVD events. Dental bacteria typically result in calcification around the roots and enamel structures called "dental plaque", an interesting coincidence. I have also seen at least one case of zero calcification on ultrafast CT scan who required intervention and stenting after experiencing an AMI within a 1-2 year interval. On individuals who have elevated calcium scores I have a number now who have gone on to have high resolutions CT arteriography and/or Thallium scans as well as arteriography (scores over 1000 or who are positive on thallium scanning. Thalliums scans are frequently negative and the high resolution scans (16-24 slice) frequently show either mixed soft and calcified plaque or primarily calcified plaque. Older stable calcified plaque may have significant collateral development while softer new plaque frequently is more likely to rupture even without previous positive thallium scans. The soft plaque may be more likely to be related to traditional risk factors whereas calcified plaque has poor correlation. Diabetics have different types of plaque and plaque erosion with less lipid core, so there are clearly different types of plaquing that may represent several differing mechanisms. I find the idea that calcium scanning does not meet the criteria for screening to be ridiculous based on over 5 years of experience. |
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December 26, 2005 08:24 (EST)
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Endothelial pathology: not just academia anymore
Eugene,
Good points. This discussion demonstrates how far we have come in our understanding of endothelial pathology. Our descriptive terminologies should include ACS as well as "CCS", chronic coronary syndrome when we are referencing patient scenarios.
A giant step in the application of this understanding includes those think tank cardiologists who believe that stenting plaque in diabetes is the way to go instead of waiting for angiographically significant disease. It has already impacted our revascularization referral patterns for diabetic patients who do better with CABG than with PCI for MVD.
The understanding of these differences has changed the way we approach our stress lab patients. Unless we translate this understanding to the lay public, we have done ourselves no favors.
I have begun to prescribe nitroglycerin more often for the patients who pass their stress exams but still have a significant risk factor profile, or elevated CRP's. We insist upon lipid followup and risk factor modification even in those patients that we only oversee stress exams . We have included on their consent forms that smoking decreases the predictive power of the exam, etc. I've also taken great pains to explain to patients that a "normal" stress exam does not mean their arteries are normal, a common belief among lay people and even some referring physicians.
Patients who present for screening are the best place to put into the practice the above information but also discussions during medical society meetings and the physicians lounge would result in significant positive changes in practice as well.
No matter how important we think we are, Cardiologists are not the front line in the wave of Prevention that should be sweeping this country. We are often merely viewed as the SWAT team for ACS. So, our best bet to translate all of this academia into lives saved is to get out there and talk about it.
Melissa
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December 26, 2005 08:58 (EST)
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We need to re-define our criteria for a good screening tool
I forgot to add my last point, then I'll get off my soap box.
Perhaps we should re-define our criteria for an adequate screening tool. To say that a six year followup didn't yield any higher events with a postive EBCT is fairly short sighted in the world of plaque physiology. Since the price tag of a 2.5hr CABG procedure is the same for a 65 year old as it is for a 75 y.o pt, we should be looking for a screening tool that yields some benefit at 10, 20, or even 30 years of life past the exam. You can't tell me that a positive calcium score in a 65 year old who is overweight, not exercising, and had untreated hyperlipidemia could not benefit from proper motivation and therapy by the time he is 75 years of age. That should be the ultimate test of a good screening tool.
Melissa |
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December 26, 2005 01:33 (EST)
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Why EBCT and not carotid plaque burden?
There is a lot of talking, thinking and working with EBCT or MSCT for stratification of risk in competion with common risk factors in predicting hygh cardiovascular risk, but ther's an other parameter " total carotid plaque burden" that is easier to have, cheaper, on hand of all cardiologist and other specialist that work with ultrasounds.
The predictive value for coronary event seems better with "carotid plaque area" than for EBCT.
I advocate a strong impulse to update many of us with this parameter, even if it's about a territory ( the carotid arteries) that are out of the usual ground of many cardiologists |
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January 8, 2006 12:09 (EST)
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What is the appropriate endpoint?
When one talks about risk stratification in primary CHD prevention and the presence of FPs, what endpoint are we discussing? Melissa seemingly talks about two different endpoints when she writes -: "So, the term false positive is really a true positive with regard to endothelial pathology, but not necessarily a true positive for significant reversible ischemia." Melissa therefore seemingly implies that one endpoint is identifiable endothelial pathology and the other endpoint is reversible cardiac ischemia. I thought that both of those endpoints are not relevant (because they are "soft" endpoints) and that the only relevant risk stratification cardiac endpoints are major MI events (fatal and non-fatal MIs). In other words, FPs should surely relate to MI events.
Secondly, Melissa writes-: "I have begun to prescribe nitroglycerin more often for the patients who pass their stress exams but still have a significant risk factor profile, or elevated CRP's." What is the purpose of prescribing NTG in asymptomatic people? I thought that NTG has only be shown to reduce the number/severity of anginal episodes in symptomatic CHD patients, and that it has not been shown to reduce the risk of a future MI event.
Jeff.
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January 8, 2006 12:38 (EST)
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how experienced publishing plaque imagers look at this
First of all, one of the reasons the Mozaffarian contention is absurd is his complaint that high calcium scores ONLY have a 15% positive predictive value over the next few years. He believes that is LOW!!! (if extended to 10 years that is way above a chd equivalent). It would be like having a high cholesterol and noting that ONLY 30% go on to have an MI in the next 10 years.
Now, the reason we speak of essentially NO false postives for calcium score, is that we are looking at atherosclerosis (PLAQUE) not obstructive CAD. It is sad that the oculostenotic reflex is so strong that cardiologists still complain that a positive score often is accompanied by a normal thallium. That is a false Negative thallium!! (Glagov remodeling). We can now say that the MAJORITY of patients who get an MI would be in the top quartile of a coronary calcium score, yet would have passed all stress tests in the weeks prior.
there is a reason that Berman's study (reported here) revealed that 94% of patients with indications for a thallium passed that test...yet a full 56% of them had a calcium score >100... a chd equivalent. So we really should be concerned that angiograms and stress test effectively hide huge plaque burdens.
the fact remains that calcified plaque is a very powerful predictor of hard events---over 10 times the CRaP test ("can't really predict" test).
I also do lots of carotid IMT using the best databases....i am impressed with its complementary value to EBT and the fact that doing both gives me a better overall picture of vascular health (and i do endothelial function testing). No test comes close to EBT calcium imaging in predicting events |
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January 8, 2006 03:48 (EST)
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Conflict of interest?
Mozaffarian totally ignorant? Shoddy work?
Here's how Dr. Ehrlich makes his living.
Conflict of interest?
Do you ask a barber if you need a haircut?
---------------------------------------
Curriculum Vitae
I. General Information/ Current Positions
Medical Director, Colorado Heart Imaging
2490 West 26th Avenue, Suite 110A, Denver, CO 80211
(303) 433-8800
Medical Director, Denver Preventive Imaging
201 Columbine St.Denver, CO80206
(303) 785-0464
Medical Director, HeartScan of Indiana
8333 Naab Road
Indianapolis, Indiana
Medical Director, HeartScan Washington DC
2401 Pennsylvania Avenue N.W. Suite LL-150
Washington D.C.20037
(202) 467-0929
Chief Medical Officer, US Preventive Medicine, Inc.
II. Current Titles and Appointments
Medical Director
Colorado Heart and Body Imaging
Denver Preventive Imaging
HeartCheck WashingtonDC
HeartScan of Indiana
HeartScan Partners
Adjunct Asst. Professor (Dept. Medicine), The George Washington University School of Medicine
Clinical Asst. Professor, (Dept. Medicine), University of Colorado School of Medicine
President, Society for Responsible Preventive Imaging
Director, Society of Atherosclerosis Imaging
Chief Medical Officer, US Preventive Medicine, LLC
Head, Medical Advisory Board, US Preventive Medicine |
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January 8, 2006 10:30 (EST)
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Gentlemen
Gentlemen,
A healthy debate is always welcome, however personal attacks really are an unnecessary distraction, so let's stick to literature and medical opinion. Also, if any of us have a conflict of interest, it might be best to just start off the discussion with that disclaimer just as we are asked to do when we are presenting.
Jeffrey,
I prescribe nitroglycerin sublingual to patients at risk because it limits ischemia in both human and animal models (by decreasing left ventricular stroke work index, reduces afterload and pre load and decreases platelet aggregation. Additionally, studies with nuclear assessment for "fill-in" with nitroglycerin help to assess viability by improving blood flow, therefore, we extrapolate) It seems like the humane thing to do. Additionally, receiving a prescription " for just in case" validates my concerns for them and will hopefully motivate them toward lifestyle change (Colin, you should appreciate this !). It also reminds them not to sit at home during their MI, if they have symptoms, affords an opportunty to discuss symptoms of an MI, etc) .(Off the subject, but It also prevents my patients who are inoperable with flash pulmonary edema from requiring intubation so I respect nitro) These are common sense tactics and I don't believe I'm alone in doing this. Doubt we'll ever design , in my life time, a placebo vs SL nitro outpatient study. I've never studied crossing a busy street with or without a blind fold, but I can guess the outcome.
James, we have to be careful about interpretation of stress exam results. Often patients with significant obstructive coronary disease are 1. on anti-ischemic and /or antiplatelet drugs during their exam, thus impacting the predictive value. 2. exercise duration is a very valuable predictor of death/MI, 3. interpreting these exams requires many different levels of assessment: which meds, how long they stressed, ECG changes, inducible arrythmias, BP progression, heart rate recovery time, etc. So just stating that many patients who have a negative thallium will go on to have events is a pretty broad blanket statement. If a hundred patients can do 13 minutes on a standard bruce protocol without reversible ischemia despite known disease, I'll bet much fewer than 50% will have an event in the next few years. However, patients who exercise only 5 minutes are much more likely to have events, despite having a negative exam.
As for EBCT, I believe it has it's place in medicine, but perhaps not for mass screening but more for directing a thoughtful workup
Melissa
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January 9, 2006 03:31 (EST)
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My understanding of Mozaffarin's paper
James Ehrlich's critical comments regarding the Mozaffarian paper in JAMA made me go and read the paper to see if Ehrlich's criticisms make sense.
I think that the Mozaffarian paper is one of the best review papers that I have ever read. It is well balanced and it is obvious that the author is fully aware of the relevant literature. I am flabbergasted at the poor quality of Ehrlich's criticisms, which may not be totally surprising considering his "apparent" conflict of interest.
First of all, Ehrlich states that Mozaffarian has zero experience in the field of EBCT and he implies that Mozaffarian is therefore not qualified to review the EBCT literature. That argument makes no sense, because the quality of a review article is primarily dependent on the extent of the reviewer's literature search and the quality of his logical reasoning when assimilating all the relevant EBM evidence. I know of no evidence that suggests that a person who actually performs EBCT can review, and analyse, the relevant EBCT literature better than a person who doesn't perform EBCT. That fallacious argument would be equivalent to saying that only interventional cardiologists can write review articles on the value of angioplasty in patients with known CHD!
Ehrlich claims that there are no FP results, and he defines a true positive result as the "presence of atherosclerotic plaque". However, what is the relevance of diagnosing atherosclerosis? How does it change patient management? Is Ehrlich arguing that all positive EBCT results mandate one therapeutic/preventative modality while all negative EBCT results require a different (or no) therapeutic/preventative modality. If so, I would like to see Ehrlich's actual recommendations and get to understand the logical reasoning connecting a positive/negative EBCT result with a particular therapeutic/preventative approach.
Mozaffarian presents a cogent argument in his paper, that is well summarised in a diagram. Basically, EBCT screening would most likely be performed on asymptomatic patients who have a 2-8% risk of a CHD event (MI or CHD death) in the next 5 years. A positive EBCT test would apparently increase that 5-year risk to 12-15%. Why would a 12-15% risk be significantly different from a 2-8% risk from an individual patient's perspective? Surely, a rational patient would base his preventative approach on his overall risk of a CHD event. For example, if he is overweight, has poor dietary habits and doesn't exercise, then it is possible that he may deem it appropriate to institute lifestyle changes if he is informed that his 5-year risk of a CHD event is ~7%. Will that individual likely have a greater incentive to institute those lifestyle changes if informed that his 5-year risk is actually 14%, rather than 7%? Does the financial expense of the EBCT justify the degree of change in risk-knowledge? In his diagram, Mozaffarian indicates that a positive EBCT result may result in further diagnostic testing, which may subsequently lead to elective coronary revascularisation. However, from previous heart.org forum discussions, I have learnt that there is apparently no EBM evidence demonstrating that elective coronary revascularisation in asymptomatic patients decreases the risk of a CHD event (compared to conservative management). Also, one has to take into account the wastefullness/risks of harm of further cardiac testing in patients who turn out not to have sufficiently severe CHD disease that could possibly warrant elective coronary revascularisation.
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January 9, 2006 03:33 (EST)
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-- part 2
-- continued from part 1.
According to Mozaffarian, 80-90% of patients (who have an overall 5-year risk of a CHD event of 2-8%) undergoing a EBCT will have a negative result, and he states that their 5-year risk of a CHD event subsequently decreases from 2-8% to 1-7%. Again, how would a negative EBCT result likely affect an individual patient's thinking? Surely, it may still be as appropriate (or inappropriate -- depending on an individual patient's values) to institute lifestyle changes if the patient is overweight, doesn't exercise, and has poor dietary habits -- if his 5-year risk of a CHD event is 1-7% rather than 2-8%?
If a patient has a higher 5-year risk of a CHD event (than average) because he has diabetes and/or hypertension, then it would presumably be appropriate for that patient to institute appropriate lifestyle changes/drug therapy -- irrespective of the result of a EBCT test. Can anyone demonstrate that a positive (or negative) EBCT result should change the appropriate preventative/therapeutic approach in an individual patient?
Mozaffarian also argues that within each Framingham risk category, that a positive EBCT result doesn't necessarily change the cholesterol treatment guideline approach. Can anyone find a flaw in his argument? Mozaffarian argues that a negative EBCT result may change the cholesterol treatment guideline approach in patients with a 10-year risk of a CHD event of 10-20%, because those EBCT-negative patients will only have a 1-4% 5-year risk of a CHD event. If correct, can anyone present a cost-effective analysis showing that EBCT is therefore a cost-effective diagnostic maneuver in that patient-subcategory?
At the end of his paper, Mozaffarian argues that EBCT may be cost-effective if a positive test result causes the patient to undertake a theraputic maneuver that reduces the CHD mortality by a finite amount (eg. 25-30%). However, I cannot understand how a positive EBCT test result could decrease the CHD mortality rate to such a significant degree in asymptomatic patients (who only have an overall 5-year risk of a CHD event of 2-8%). What therapeutic modality (following a positive EBCT result) could result in such a significant mortality benefit?
Jeff.
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January 9, 2006 11:26 (EST)
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NTG use in asymptomatic patients
Melissa -- you write-: "I prescribe nitroglycerin sublingual to patients at risk because it limits ischemia in both human and animal models (by decreasing left ventricular stroke work index, reduces afterload and pre load and decreases platelet aggregation. Additionally, studies with nuclear assessment for "fill-in" with nitroglycerin help to assess viability by improving blood flow, therefore, we extrapolate) It seems like the humane thing to do."
This thread discussion is mainly focused on low risk patients who may/may not be suitable for a screening EBCT exam. I presume that we are talking about prescribing NTG to asymptomatic people, who have a risk of a future CHD event in the next 10 years of somewhere between 0-20%. I agree that NTG works by reducing preload/afterload, and that it can decrease anginal symptoms in the presence of a fixed coronary artery obstruction. However, I know of no evidence that it can prevent a future hard CHD event (MI or CHD death). Therefore, I think that NTG only has a SYMPTOMATIC role if the patient actually has anginal symptoms, and that there is no rationale for using the drug prophylactically in asymptomatic patients (who may not even have CHD).
You also write-: "Additionally, receiving a prescription " for just in case" validates my concerns for them and will hopefully motivate them toward lifestyle change (Colin, you should appreciate this !). It also reminds them not to sit at home during their MI, if they have symptoms, affords an opportunty to discuss symptoms of an MI, etc)".
Could you explain your reasoning further? I simply cannot understand the rationale of prescribing a medication for a condition (angina) that has not occurred, and may not occur, on the presumptive basis that it may induce lifestyle changes that can theoretically reduce the patient's risk of a future CHD event. I have never heard of that practice-idea. Also, I cannot understand how it would remind the patient not to sit at home when the patient has his first MI. Are you telling your patients to take NTG whenever they have acute chest pain and to immediately seek medical attention if the pain is not resolved within a finite time period eg. 5-10 minutes. It would seem to me that such a recommendation may cause more harm than benefit. First of all, if the chest pain episode is due to ACS, and not angina, NTG may not relieve the pain and it may actually be deleterious if the patient has an inferior MI which requires a higher preload (NTG may induce hypotension and subsequent syncope). Secondly, if NTG offers some pain relief in an ACS patient (by decreasing preload/afterload), the patient may incorrectly think that he does not have a MI. Thirdly, there is no correlation between NTG-induced pain relief and the likelihood of an ACS event in an acute chest pain patient (the diagnostic likelihood ratio for ACS is close to 1.0, and it therefore does not change the pretest probability of ACS). Fourthly, if the acute chest pain episode is completely relieved by sl NTG therapy, the patient may incorrectly presume that he had some type of CHD event, when it is equally likely that the cause of the acute chest pain may be non-cardiac eg. due to acid reflux and secondary esophageal spasm.
Jeff.
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January 9, 2006 07:56 (EST)
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Common sense still goes a long way, believe it or not
Jeffrey,
I have been prescribing nitroglycerin for 17 years. I am aware of very few patients who took the medication and required hospital admission for syncope. Perhaps it's because I always tell my patients to sit or lie down with the first dose. I will continue to prescribe nitroglycerin for some subsets of at risk patients with normal stress exams as stress testing will miss 15% of patients with high grade fixed obstruction. (There is a statistic for you!) Occasionially a patient will not comply with a recommendation for cardiac cath, yet they are willing to medicate and perform stress. I'm concerned when I strongly suspect CAD in that case and hope they aren't going to be an out of hospital sudden death. I validate my concern by giving them nitroglycerin and say to them: If you continue to have chest discomfort and if it is increasing in frequency, utlize prn nitro and please change your mind about having a cath. We've all done it.
Sometimes, you just can't justify a practice with statistics. Medicine continues to be an art, no matter how much we try to turn it into pure science.
Since smoking was invented in South Central Ketucky, we get a lot of folks with myocardial infarction but no significant fixed obstruction. So, another reason to consider nitroglycerin on occasion.
"I can't explain why we would prescribe a medication for a condition that has not yet occurred". Jeff, I haven't waited for my first MVA to wear my seat belt. That is about as clear as I can make this argument. But, I'll try in medical terms. Explain to me why arterial vasodilitation would not help ischemia with ACS. (Do you have a study to prove that it can't? ) It probably won't help a totally occcluded vessel, but it might improve collateral flow. It might buy time to V-fib. It might prevent worsening pulmonary edema. Iv nitro limits infarct size so we might extrapolate even though there may be no statistics to prove it.
NTG certainly helps in the cath lab to improve TIMI slow flow during PCI. Why would you not err on the side of patient safety? I hope you are not with holding nitroglycerin for lack of a study. Every now and then just understanding simple human physiology is enough to change or modify a practice.
As far as RV infarcts go, who can tell where there MI location is, so I won't be with holding nitro because the patient can't identify which coronary is the culprit while he's home waiting for EMS. Just who would you prescribe nitroglycerin for anyway since just about every patient scenario seems to be contraindicated in your opinion?.
Back to EBCT, which is where this entire discussion originated, and yes it's applicable to discuss therapies and prevention, follow up etc. here on this thread, I still insist that it can be a good screening tool for some, especially elderly patients with a need to avoid cath. If negative, I'm somewhat reassured.
There again, clinical acumen which has always served me well seems to work best and far better than any statistical analysis.
Melissa
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January 10, 2006 11:12 (EST)
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NTG side-issue
Melissa -- I suspect that you didn't quite understand my position about NTG use. I do NOT oppose the use of NTG for patients who have anginal symptoms, even if they have not had a cath to definitively prove that they have severe CHD. So, if a patient has classic angina symptoms on effort, pain relieved by rest and/or NTG, then it makes sense to prescribe NTG for that patient. I also do NOT oppose the use of NTG for ACS or cardiogenic pulmonary edema. I only cannot understand the rationale of prescribing NTG "just in case" a patient has an future episode of acute chest pain under the following circumstances -- If one has an asymptomatic patient that has never had chest pain symptoms, but has an estimated 10-20% 10-year risk of a future CHD event, then I cannot understand the rationale of prescribing NTG for that patient "just in case" he develops an episode of acute chest pain at some point in the next 10 years. My reasons were delineated in my previous post, and mainly relate to the diagnostic LR of 1.0 for angina, and the high incidence of FP and FN results.
You don't need to respond to this NTG side-issue. I am more interesting in discovering how people can justify the use of ECBT as a screening tool with a detailed explication of how it alters preventative treatment recommendations that are based on the Framingham risk score.
Jeff.
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January 10, 2006 11:52 (EST)
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Does failure to meet criteria for principles of screening = unhelpful?
Jeff,
I understand your interest in EBCT stastical analysis , but as a clinician, prescribing nitroglycerin or not, increasing a statin dose or not, recommending a stress exam or not or recommending a cath or not are all direct results of utilizing yet another "screening" tool such as EBCT. I can tell you already that EBCT is already being utilized by physicians as a screening tool . What you are asking is whether or not it will meet criteria for approval for mass screening and therefore will impact insurance reimbursement or impact medicare reimbursement. Probably not as it would be far too costly. There are other factors at work that determine approval for mass utilization besides whether or not it is efficacious. I think that time will tell.
Since large numbers of asymptomatic patients are dying each day of undetected CAD, mass screening of asymptomatic "at risk" patients is exactly what we need. (GASP!)
Also, I will point out that I will make the determination as to which posts I will respond to.
You need not respond to this post if you feel it is unworthy of your time or outside of your clinical experience.
Melissa |
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January 11, 2006 12:02 (EST)
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Let's remember the purpose of the Forum
Hi,
Please allow me to echo and support Melissa's last post. This forum, like this site, is designed primarily for the use of cardiovascular health care professionals. This is really not the right place (forum!) for some of the discussions that take place here.
We encourage a free exchange of ideas, but this forum can not be covnerted or subverted into an opportunity to endlessly assault mainstream cardiovascular medicine. We fully support the free expression of ideas and opinions, but there's no reason these ideas and opinions need to be endlessly repeated here.
Best,
Larry Husten
News & Features Editor
TheHeart.Org
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January 17, 2006 06:51 (EST)
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Very depressing work
From online Circulation (mainstream cardiovascular medicine).
Dr. Ehriich now has a reason to be very depressed. Suggest he take up another line of work.
Looks like Mozaffarian was right. What's the point in doing EBCT in asymptomatic patients if putting them on a massive dose of Lipitor makes zero differnce. If we accept that EBCT is really showing plaque then Lipitor doesn't work. On the other hand if we believe that Lipitor works then EBCT is not showing real plaque. Can't have it both ways.
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Background—Recent clinical trials have suggested that intensive versus standard lipid-lowering therapy provides for
additional benefit. Electron-beam computed tomography provides the opportunity to quantify the progression of
coronary artery calcification (CAC) in serial measurements.
Methods and Results—In a multicenter, randomized, double-blind trial, 471 patients (age 61 8 years) who had no history
of coronary artery disease and no evidence of high-grade coronary stenoses ( 50% diameter reduction) were
randomized if they had 2 cardiovascular risk factors and moderate calcified coronary atherosclerosis as evidenced by
a CAC score 30. Patients were assigned to receive 80 mg or 10 mg of atorvastatin per day over 12 months. Progression
of CAC volume scores could be analyzed in 366 patients. After pretreatment with 10 mg of atorvastatin for 4 weeks,
12 months of study medication reduced LDL cholesterol from 106 22 to 87 33 mg/dL in the group randomized to
receive 80 mg of atorvastatin (P 0.001), whereas levels remained stable in the group randomized to receive 10 mg
(108 23 at baseline, 109 28 mg/dL at the end of the study, P NS). The mean progression of CAC volume scores,
corrected for the baseline CAC volume score, was 27% (95% CI 20.8% to 33.1%) in the 80-mg atorvastatin group and
25% (95% CI 19.1% to 30.8%) in the 10-mg atorvastatin group (P 0.65). CAC progression showed no relationship
with on-treatment LDL cholesterol levels.
Conclusions—We did not observe a relationship between on-treatment LDL cholesterol levels and the progression of
calcified coronary atherosclerosis. Over a period of 12 months, intensive atorvastatin therapy was unable to attenuate
CAC progression compared with standard atorvastatin therapy. The possibility remains that the time window was too
short to demonstrate an effect. (Circulation. 2006;113:427-437.) |
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