First comes the patient. If there are no complaints there is no indication to perform a coronary CT. If there are symptoms suggestive of a coronary problem even if the CT shows no calcifications I would strongly recommend to procede with the appropriate investigations (e.g. stress testing ,radionuclid scanning etc.

In summary ,I,see no need to itroduce this procedure into standard clinical practice.

Hi Bernardo. Coronaries artery calcification detected with the new generation of Eco Doppler, and moreover, as evidence between adventicial and intimal calcification detected in a syntomatic old patient, are markers of, at large, adverse events.

Dear colleagues,

It is a very interesting question. Unfortunately I do not knonw where is the place of CT in clinical practice. Moreover, calcium identification could be a nice tool for stratifying cardiovascular prognosis. But we have no enough evidence in this setting.

I aggree with all of the above answers. While coronary calcium sometimes helps us plan appropriate device selection for coronary intervention, the mere presence of calcium means an abnormal coronary and therefore has all the attendant prognostic implications. It does not in and of itself say anything about physiology or degree of stenosis. One might re-double your risk factor modification strategy, knowing a calcium score, however this has not yet been demonstrated to give the same information that a routine exercise stress test does.

Yes. However, the most reliable result is zero score. Those I do not refer to angiography or similar, whereas high values along with suspect anamnesis often triggers supplemental angiogeaphy.

Not quite. There are a lot of studies that show a direct relation between stoke or cardiovascular events with the presence of artery calcification. In this respect, local (MGP) or circulating (fetuin) calcification inhibitors are studied extensively.

If the question is about decision making for the PCI strategy then I would say yes, as already answered by Bernardo. Intravascular Ultrasound (IVUS) is very helpfull to analyse the angle of calcium and wheter it is intimal (superficial) or adventitial (deep) calcium and the location in the coronary artery. One can imagine that a > 180 degrees "napkin" ring of superficial calcium may require a technique like rotablator to prepare a lesion before implanting a stent.

Not for a routinely basis. It could be useful in specific situations, as in type 2 diabetic patients as a first step before going to SPECT for detection of silent ischemia (there is one algorithm proposed by Anand D et al. Eur Heart J 2006;27:713 that explains this). For risk stratification in other types of asymptomatic individuals is not really established as far as I know.

Amalia Peix

In severely calcified vessels, intravascular imaging modalities, notably optical coherence tomography (OCT),can help with PCI strategy (examples: usage of calcium modification devices like rotablator and cutting ballons) as the depth of the calcification, which is a crucial element that predicts the effectiveness of these devices, can be clearly demarcated by OCT.

I agree with Emile Mehana. The presence of high coronary calcium score would make the requirement for rotablator more likely. This would ensure the use of such a device as an elective procedure rather than after failure to negotiate or dilate with a balloon. CT calcium scores can probably be obtained when coronary angiogram shows calcified lesions

CT detects all major vascular calcification and gives "definite evidence for coronary atherosclerosis" however, these heavily calcified lesions are usually stable. More apealing is the detection of micro calcification in prognostic relevant vulnerable plaques. Unfortunately does not even ex-vivo micro CT pick up these micro calcification reliably. Way to go.

There seems to be a lot of confusions as to the role of CAC scanning in clinical practice as noted by the above answers. While there may be a role of calcium scanning in acute chest pain or in planning intervention, that is not where it should be used for clinical decision making. It is best used as a way to assess cardiovascular risk in asymptomatic patients. It is the only way to non-invasively assess the presence of non-obstructive disease in the coronaries. Exercise tests, nuclear and echo all require the presence of an obstructive lesion to be abnormal. Standard risk factors such as lipids, HTN etc. do not tell you what is happening in the coronaries. The majority of MACE events occur in patients with normal cholesterol levels. When assessing a patient for possible lipid lowering therapy the presence or absence of calcium, as well as the total calcium score is extremely helpful in deciding whether or not to treat and how aggressive yo be. The evidence is overwhelming at this point of the added predictive value of CAC scoring to risk assessment. There will probably never be a randomized clinical trial showing the survival benefit from aggressive treatment in patients with high calcium scores given the cost, time and ethical issues that would be involved in not treating patients with high calcium scores, but that does not mean that you should not use the existing data to guide your decision making.

Many thanks for discussants. Clearly, various aspects of CAC scoring have been touched that considered different populations (asymptomatic persons, symptomatic patients at the ER, symptomatic patients scheduled for PCI).

First of all, the presence of coronary atherosclerosis by means of CAC is almost exclusively the evidence of an “iceberg below the water”. As a substantial proportion (~50%) of coronary events, including sudden death and/or myocardial infarction (symptomless, symptomatic fatal) occurs in seemingly healthy persons, who have actually coronary atherosclerosis, awaiting for the occurrence of symptoms or signs of ischemia might be a time-consuming and ineffective process. One has to consider specificity and sensitivity, as well as reproducibility and robustness of the proposed diagnostic methods. As the CAC can be performed in actually all persons, each of ischemia detecting method has its own limitations. In other words, the detection of CAC is a proof for subclinical coronary artery disease, not a risk factor. Alternatively, it’s basically the stable coronary artery disease. Accordingly, some medications should be administered along with recommendations for stable CAD treatment, including statin (if LDL level is higher than 100mg/dl, acetylic acid (if not clearly contra-indicated), ACE inhibitor (irrespective of blood pressure), and, if necessary a beta-adrenolytic agent (if HR > 80 bpm), as well as implementation of non-pharmacological preventive measures (diet, physical activity, smoking cessation in smokers). A counseling regarding drug-adherence does seem mandatory. Searching for non-coronary atherosclerosis is necessary, as the number of vascular (non-coronary) lesion territories influence the outcome (sudden death, MI, stroke, aortic aneurysm).

Second, any CAC lesion located within LM, proximal LAD, proximal part of other dominant artery should be further evaluated by means of invasive coronary angio, OCT and/or IVUS. A dense CAC within proximal coronary artery brings 4-16-fold greater risk of mortality than dispersed high CAC within the entire coronary tree. The same rule regards patients with and without diabetes mellitus.

Third, the evidence of CAC must not influence outcome, as there are a proportion of patients with coronary artery lesions at autopsy who died for other reasons. Also, a high CAC score detection in octogenarians indicates that stable CAD might develop slowly and cannot account for coronary risk (as the CAD as a killer affects persons within 50-65 years, with a 10-year period’ shift in non-smoking women i.e. 60-75 years of age).

To be smart, CAC scoring should be started in asymptomatic men at age of 40 (if at least one traditional risk factors is present, i.e. systemic hypertension, high lipids, diabetes, family risk, smoking) and in asymptomatic women at age of 50 (same conditions). Medical (pharmacological and non-pharmacological) approach might be therefore mandatory. X-rays exposure might be considered insignificant (CAC < 1milliSieverts) taking into account that there is no other method for a straight coronary atherosclerosis evidence.

If a subject is symptomatic, there are data indicating that age and gender are the solely factors that might be helpful (see Diamond-Forrester algorithm with its improvements). CAC scoring might be a gatekeeper for invasive coronary angiography, however data is sparse and the evidence not confirmed in a randomized fashion. The same regards the choice of PCI strategy.

M.Sosnowski

I agree with most of Dr. Sosnowski's comments above except for the need to do invasive coronary angio when LM or proximal calcification is present, particularly in asymptomatic patients. I'm not aware of data showing a 4 -16 fold risk of mortality in these patients. Do you have a reference? There is also no data that I am aware of showing improved mortality if these patients have intervention. In general most patients whould not have invasive studies based on a calcium score. Some may benefit from non-invasive testing for silent ischemia. Intensified medical therapy should be instituted in patients with high calcium scores, particularly those in the highest percentile for age, gender and ethnicity. I would extend this even to patients with LDL's less than 100ml/dl, though there is not good data to support this.

CAC should be used like a Framingham risk factor. For those on the cusp of having statins prescribed due to their overall 10 year risk a calcium scoring could be performed and change the risk significantly. The exact calcium score can give you their "arterial age" which can be substiuted for their chronological age when perfoming the risk calculation by whatever method you routinely use. eg Anyone with a calcium score of 0 has an arterial age of

Lot has been said and done about coronary calcium. The context is the most important factor. For risk stratification in asymptomatic individuals it is an incremental info (0 = very very low risk). In symptomatic, acute, and so forth it is a completely different situation.