Edinburgh, Scotland - Measurement of the ankle-brachial index (ABI) may improve the accuracy of cardiovascular risk prediction beyond the Framingham risk score, a new meta-analysis suggests [1].
The analysis, published in the July 9, 2008 issue of the Journal of the American Medical Association, was conducted by a group led by Dr Gerry Fowkes (University of Edinburgh, Scotland).
Fowkes commented to heartwire: "Evidence is slowly accumulating that the ABI is a good risk marker in addition to Framingham. Our paper will advance that notion further." He added that while doctors could currently use an ABI score alongside the Framingham risk scores, a more accurate result would be obtained from an equation incorporating both scores together. "To produce such an equation, you have to have a large data set. We have now got such a data set and are hoping to formulate and validate a model including both scores within the next 12 to 18 months," Fowkes said.
In the paper, the authors explain that predicting future risk of heart disease and mortality accurately in individuals in the community who have no prior history of cardiovascular disease has proven difficult when based solely on traditional risk factors and scoring systems. For example, in a recent systematic review of 27 studies using the Framingham risk equation, the predicted-to-observed ratios ranged from an underprediction of 0.43 in a high-risk population to an overprediction of 2.87 in a low-risk population.
Fowkes et al note that the incorporation of other risk markers, such as metabolic syndrome and C-reactive protein, has had partial success in improving prediction, and attention is also being given to indicators of asymptomatic atherosclerosis, such as coronary artery calcium, carotid intima media thickness, and the ABI, which is the ratio of systolic pressure at the ankle to that in the arm. They add that the ABI is quick and easy to measure and has been used for many years in vascular practice to confirm the diagnosis and assess the severity of peripheral artery disease in the legs.
The authors report that a low ABI has been related to an increased incidence of mortality, MI, and stroke in population studies. They set out to establish whether the ABI provides information on the risk of cardiovascular events and mortality independently of the Framingham risk score and can improve risk prediction. To do this, they conducted a meta-analysis of 16 population cohort studies in which participants were derived from a general population, ABI was measured at baseline, and individuals were followed up to detect total and cardiovascular mortality. The studies included a total of 24 955 men and 23 339 women.
Results showed that a low ABI (0.90 or less) predicted vastly increased risks of 10-year cardiovascular mortality in both men and women.
10-year cardiovascular mortality (%) according to baseline ABI
Group
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Low ABI (<0.90)
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Normal ABI (1.11-1.40)
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Men
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18.7
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4.4
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Women
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12.6
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4.1
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To download table as a slide, click on slide logo above
The risks remained elevated after adjustment for Framingham risk score, with a low ABI associated with approximately twice the 10-year risk of total mortality, cardiovascular mortality, or major coronary events compared with the overall rate in each Framingham risk score category.
Fowkes et al report that inclusion of the ABI in cardiovascular risk stratification using the Framingham risk score would result in reclassification of the risk category and modification of treatment recommendations in approximately 19% of men and 36% of women. However, this proportion may vary considerably by age, because the prevalence of a low ABI is known to increase substantially with age. While the main effect of the ABI result in men would lead to some individuals who are currently thought of as high risk having their risk downgraded, the main effect in women would be that many at low risk with the Framingham score would change to a higher risk level, they say
The authors further point out that in contrast to measurement of coronary artery calcium and carotid intima media thickness, measuring ABI is much easier to do in the primary-care physician's office and in community settings. They note that the equipment is inexpensive, with a handheld Doppler costing less than $600; the procedure is simple, taking less than 10 to 15 minutes and able to be performed by a suitably trained nurse or other healthcare professional; technological advances to make the test quicker and easier to apply are being investigated, including automatic pressure measurement at the ankle; and, given the noninvasiveness of the test and minimal discomfort, patient acceptability is high.
But they say that despite all these advantages, ABI is rarely applied in routine clinical practice, as most clinicians are not aware that a low ABI is a marker of cardiovascular risk and would not know how to perform the test. Therefore, physician education would be essential in promoting use of the ABI in practice.
Source
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Ankle Brachial Index Collaboration. Ankle brachial index combined with Framingham risk score to predict cardiovascular events and mortality. A meta-analysis. JAMA 2008; 300:197-208.
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What about Inherited Real Risk of CAD? Unfortunately the authors, Editors and Reviewers overlook (NOT ignore...) Inherited Real Risk of CAD (www.semeioticabiofisica.it, Practical Applications and Bibliography). |
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Abnormal ABI = advanced disease This report is nothing more than another indictment of using Framingham for clinical risk assessment. Yet another observation that a subset of patients will develop advanced atherosclerosis despite being Framingham low risk is all the more reason to find and apply a more accurate, more precise, and more useful tool to stratify risk. EBT-CAC does come to mind.
Framingham is a great study from which we have learned and continue to learn a great deal. Treating Framingham risk factors is appropriate. Relying on Framingham to determine who is at risk is a fatal mistake.
A question I have is how many ways are primary care physicians expected to assess risk. Start with Framingham, add family history, add ABI, measure 6 or 7 novel blood tests, put it all together and guess. Alternatively, they could do an EBT CAC for less cost than the above and get a result many times more accurate,and also provide a baseline for future comparison to measure adequacy of interventions.
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ABI utilization: It's not about education only! In Europe, many healthcare systems do not reimburse ABI testing for GPs. In the UK as Dr.Fowkes knows, PAD as a whole is not even part of the QoF system. So it's not only about physician education |
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Correlation ABI and PAD in Asian Countries in PAD searc study (2006), PAD is common in Asian Type 2 Diabetes patients, but in Indonesian people is very difficult to ABI testing for GPs. The ABI machine is very expensive. I think public awareness or education program from physician is very important to us. |
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But you can still detect PAD without it Bambang,
I know the ABI apparatus is ideal, but you can just check a thigh and brachial pressure and if no thigh cuff available, just palapating pulses and listening for bruits beats nothing. I only point that out because so many folks don't ever get their pedal pulses checked and it amazes me how many physicals they may have had, but never had their PAD detected. Since 1 in 4 of these patients will be dead of myocardial infarction in 5 years, it's of the utmost importance.
Thanks for your post.
Melissa |
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July 10, 2008 02:04 (EDT)
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Sequential testing, but which test? Framingham risk, especially within the intermediate range (6-20) needs refinement in order to reclassify subjects into other risk categories. CAC? ABI? IMT? CRP? I have tried them all and ended up with carotid plaque imaging (total plaque area, tpainfo.ch). It detects high risk subjects much earlier than ABI, is frequently positive when CAC is positive (dta on file), is done rapidly without any radiation burden and is better than IMT (see Tromso study). Integration of TPA in clinical risk management is straight foreward with posttest risk calculations (Bayes formula, scopri.ch). Do not wait until ABI becomes positive. And show the images to your patients. They will understand immediately. |
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July 10, 2008 09:03 (EDT)
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| Pedro Enrique Miguel Soca |
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CVD Predictor It is a new predictor of Cardiovascular Disease, but I prefer the classical indicators as C-LDL and C-HDL. We need more investigations about this index. |
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July 10, 2008 11:43 (EDT)
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MESA This is an ongoing trial looking at several non-invasive screening tests for ASCVD. The question is, which one is best? How do you define best? Least expensive, least risk to patient, most sensitive? Then there's the question of incremental benefit of multiple screening modalities. What about a combination of modalities used as an index, such as CAC (nod to W. Blanchet) + ABI + CIMT? |
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July 10, 2008 01:58 (EDT)
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Answer not finished yet The answers to Dr. William Dixon questions as we know, aren't finished yet, this is why all this debate continues. Nowadays there aren't data enough to change from primary prevention from Framingham to CAC score for example, except in a particular group of moderate risk ones. With respect, but there's yet a lot of data questioning the conduct suggested by Dr. William Blanchet, just above. |
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July 12, 2008 12:20 (EDT)
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statins in the water We know from AFCAPS/TEXCAPS that low LDL-C and low hs-CRP have very little risk o/w we should put statins in the water so we can all be like the PCSK9 mutants. Extra tests are really only helpful in getting pts on board. |
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July 12, 2008 02:24 (EDT)
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Statins in the water? If we put statins in the water we will only prevent 33% of the heart attacks and atherosclerosis will continue to cause more deaths than the all cancers, accidents and infections combined. What we really need is a test to find out who is truly at risk and then measure serial testing to see when we have successfully countered that risk. Such a test does exist however; the cardiology world would prefer to stay true to high science than to look at the preponderance of the DATA and make an intelligent decision. |
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July 12, 2008 02:26 (EDT)
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What DATA questions my conduct? Guiliano, please explain your comment. What DATA causes you to question my conduct? Please illuminate. Is there an issue with preventing heart attacks and saving lives that I am missing? |
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July 15, 2008 12:28 (EDT)
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Giuliano, either provide documentation or apologize It is wrong for Giuliano Bortoluzzi to make a statement as he did in post #9 and not back it up with references. This is typical of how our medical "leaders" have responded to EBT imaging. Sadly, making libelous statements supported by no evidence or knowledge is more the norm than the exception when it comes to EBT-CAC imaging comments by cardiologists.
Our comfort with our currently failing technology where we ignore the majority of individuals at risk by limiting prevention to “Framingham risk stratification” defies explanation. Treating to prevent <40% of the events with NCEP-III is also an outcome that I cannot consider adequate. Furthermore, we continue to focus on looking for and correcting obstruction even though it is well documented that non-obstructive disease causes over 80% of heart attacks. This obstructionist approach is at the expense of effective prevention with adjustment of the physiology which caused the plaque to develop in the first place.
I describe a technology that has changed my practice and dramatically reduced heart attacks and strokes in my large Internal Medicine practiced and I am subjected to the jeers of people such as Giuliano and others. Yesterday, I saw 6 patients with advanced coronary disease, none of whom qualified for cholesterol management by NCEP-III. They were all found by EBT imaging and all went from “low risk” by Framingham to “high risk” by EBT-CAC. Four out of the six have stable plaque doccumented by serial EBT imaging demonstrating adequacy of prevention.
One of the patients I saw yesterday has PAF. After getting an ablation, he had a CTA to look for pulmonary artery stenosis. They used coronary CTA protocol and incidentally found a 70 to 80% obstruction in the mid LAD. In this asymptomatic patient who has recently passed a nuclear stress test, has stable plaque by serial EBT and who is not limited with any physical activities was recommended to have an angiogram and stent of this lesion. Here is the irony; the EBT-CAC which discovered his disease and has guided me to alter his treatment to one that has successfully stabilized his plaque is not covered by insurance. If he proceeds with the angiogram and stent, despite the fact that all available literature would suggest that the stent would not reduce his risk for an MI and would likely increase his risk, the insurance company would pay for the stent without question. And I am the one that Giuliano criticizes!
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July 15, 2008 11:04 (EDT)
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ok, so should we EBT all abis? I tend to agree with the utility of EBT screening but I wonder if I should be doing this eval in every patient with abnormal ABIs? This study, although interesting, doesn't tell us where to go next in terms of workup. If the abis are abnormal, should we then do a. a nuc stress, b. stress echo, c. EBT-CAC, d. cath???????? I know that I have been much more aggressive in ABI screening in my patients, most of whom have established cad. |
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July 16, 2008 08:06 (EDT)
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advanced lipid testing Another front to add to screening should include apolipoprotein number and analysis with a reproducible and regulated modality. VAP only reproducible 40% of the time. NMR and Berkeley are vrey expensive. I agree that CAC screening has a utility in the intermediate risk FHS patient and is more reproducible and less user dependent than CIMT. There is no single right or wrong answer. I think we all are searching for the holy grail for prevention of the 30-40% who first present with CAD and SCD.
We are implementing our techs to do BP in both arms and ABIs on patients per USPTF recommendations. Only problem is back log of patients in waiting room as tech gets ABIs when patients are scheduled in 15 minute slots.
Statins in water has potential. But as an example, 45 yo male with MI and family history with "normal lipids" and no other risk factors. Had an Lp(a) of 100 nmol/L (<75 is top normal). Does not benefit from statins since statins don't work on Lp(a). His LDL is already 68. So I added Niacin. Just an example of some, but not all of patients we are capable of finding the missing link.
I commend all those in this blog who continue to discuss and challenge our current screening guidelines, since although we may disagree on find points (CIMT, CCS, etc) we all agree that we can and have to do better with CAD prevention.
Daniel |
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July 16, 2008 03:33 (EDT)
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What do you do next if you get a normal ABI? Don't stop there. According to ACC/AHA Guidelines for the Management of PAD JACC Vol. 47, No. 6, 2006 Hirsch et al. March 21, 2006:1239–312 Available at:
An exercise ABI measurement can be useful to diagnose lower extremity PAD in individuals who are at risk for lower extremity PAD (See patient risk factors below) who have a normal ABI, are without classic claudication symptoms, and have no other clinical evidence of atherosclerosis.
An Active Pedalplantar flexion (APP) / tiptoe raise test could be performed if the patient is not phyisically capable of walking on a treadmill or your office does not have a treadmill available.
Consider a Treadmill ABI in these patients at risk with normal ABI:
Individuals at Risk for Lower Extremity Peripheral Arterial Disease
● Age less than 50 years, with diabetes and one other atherosclerosis risk factor (smoking, dyslipidemia, hypertension, or hyperhomocysteinemia)
● Age 50 to 69 years and history of smoking or diabetes
● Age 70 years and older
● Leg symptoms with exertion (suggestive of claudication) or ischemic rest pain
● Abnormal lower extremity pulse examination
● Known atherosclerotic coronary, carotid, or renal artery disease |
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July 16, 2008 04:09 (EDT)
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Answering Dear Dr. Blanchet.
First of all, putting your opinions in a discussion forum opens up the possibility of reading on another day, opposite ones and even critics to your point of view. I don’t owe any apologies to anyone in this forum as I’m not acting disrespectfully or unethically and above all, my opinion is not a wrong one based on nowadays data.
Second, I’ve just passed some busy days working and only entered the forum again today, justifying my this three days without answering you.
I hope we can erradicate SCD one day, but at this time the biggest part of your point of view and way of conduct are still to be proven and I remember you that a one man experience nowadays cannot be used as consensus.
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July 16, 2008 04:13 (EDT)
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Answering 2 I wrote “With respect, but there's yet a lot of data questioning the conduct suggested by Dr. William Blanchet, just above”.
I’ll explain: when you wrote”… apply a more accurate, more precise, and more useful tool to stratify risk. EBT-CAC does come to mind”, you’re almost indicating this conduct as it was an already proven one for all patients. You didn’t wrote “moderate risk patients” or “selected cases”, and as I’m really critical, I had to write down that opinion, that for sure you didn’t like.
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July 16, 2008 04:15 (EDT)
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Answering 3 Than you wrote “Alternatively, they could do an EBT CAC for less cost than the above and get a result many times more accurate, and also provide a baseline for future comparison to measure adequacy of interventions.” Alternatively, in my view is affirming in “changing from one to another”, and i’m sad to repeat that this conducts aren’t yet proven, at all.
Relying on evidence-based medicine you can’t transfer screening from scores as Framinhgan or Euroscore, for example, to CAC-Score, exclusively, and that’s what you’ve written. You can check by yourself again in #2. Sorry but I have to disagree with that.
What is the better answer to CAD prevention, SCD prevention, probably is the association of it all, although difficult to do. But it is not proven nowadays that you should rely only on CAC score, as you wrote.
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July 17, 2008 12:51 (EDT)
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Thank you Giuliano I appreciate your reply. I also respectfully disagree when you say "there is a lot of DATA questioning the conduct suggested by Dr Blanchet". There are opinions that disagree but there is no data showing that my position is wrong. ST Francis Heart Study and the recent MESA study have demonstrated that CAC is an independent and incremental risk factor better than all other risk factor assessment. That is the fact, everything else is opinion. There is a major difference between stating that there is evidence proving something wrong vs there is inadequate evidence supporting that position. One might argue that there is inadequate evidence supporting my opinion (using foolishly strict criteria for adequacy) but to state that there is “a lot of DATA questioning the conduct” is simply untrue.
It has been stated that a series of anecdotes does not constitute a study. I beg to disagree. We have determined that it is dangerous to drive drunk, not based on a prospective controlled study but rather on a series of anecdotes. Similarly when I daily see patients with advanced heart disease found only by EBT-CAC, I am forced to similarly conclude that there is value here. Furthermore, when vascular events have all but vanished from my practice, I am forced to conclude that there is value in what I do.
I saw a 50 year old male with normal cholesterol who had undergone normal stress testing for years who today had an EBT-CAC score of over 1,000 placing him in the 98th percentile for age and ultra high risk for an MI. He will now be given the benefit of improved primary prevention and will statistically enjoy reduced risk for a coronary event. Today I also saw a 64 year old woman who had a normal angiogram 2 years ago with a calcium score now placing her in the 96th percentile for age. Again, we were able to identify someone who needs more effective treatment than she has historically received. This happens every day. We don’t need a large prospective study to know that driving drunk is a problem; furthermore this study can never be done. When the anecdotal evidence is as overwhelming as it is with calcium imaging, it is equally foolish to insist on a prospective, blinded study (that also can never be done) before we begin using it. We have never done a prospective blinded study showing value of stress imaging, angiography or echocardiography showing value yet we still use them.
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