The power of zero calcium score: Is there a need for improvement?
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Department of Cardiology, Inselspital, Bern University Hospital, University of Bern, Switzerland
Bern,
Received Jul 30, 2020; accepted Jul 30, 2020 doi:10.1007/s12350-020-02326-7
See related article, https://doi.org/10.10 07/s12350-020-02247-5.
The early detection of coronary artery disease (CAD) is key for effective therapy decision-making to lower morbidity and mortality. Thus, the cardiovascular community made huge efforts to find optimal ‘‘gatekeeper’’ methods. A promising tool is the coronary artery calcium score (CACS), also called Agatston score,1 which allows visualization and quantitative assessment of calcified coronary atherosclerosis in native computed tomography, without the need of a needle or contrast agent.2,3 Thirty years after its introduction1, CACS has emerged as the most predictive single cardiovascular risk marker in asymptomatic individuals, allowing preventive treatment modification in a selected population with borderline-to-intermediate atherosclerotic cardiovascular disease (ASCVD) risk (i.e., estimated risk of 5-20%).4 Consequently, its application has been implemented by the guidelines5 in asymptomatic individuals. However, CACS is not (yet) recommended in symptomatic patients, although evidence exist of its excellent risk prediction, as recently shown by a meta-analysis of 34,000 patients with stable chest pain.6 Advantage of CACS is the following: It is a fast, low-cost, low-radiation test that allows in the absence of calcifications the exclusion of CAD with a high sensitivity (also known as ‘‘the power of zero’’). Therefore,
Funding None. Reprint requests: Christoph Gra¨ni, MD, PhD, Department of Cardiology, Inselspital, Bern University Hospital, University of Bern, Freiburgstrasse 18, 3010 Bern, Switzerland; christoph.graeni@ insel.ch J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2020 American Society of Nuclear Cardiology.
CACS represents an ideal CAD—rule out test with a high negative predictive value, and can reclassify individuals in a high number. However, there are several shortcomings of the CACS. As stated by David E. Newby, ‘‘coronary artery calcification is a proxy of disease because it is induced in response to atherosclerosis’’ and represent an adaptive healing response of the body to limit the atherosclerotic disease.7 Are we too late in the process of imaging CAD by using CACS? We might indeed miss the early phase of CAD, and the most vulnerable plaques, the formation of non-calcified plaques (also known as ‘‘low-attenuation plaques’’ or ‘‘soft plaques’’) in a native computed tomography. In addition, stenosis grading is not possible, no information on myocardial perfusion is available, and therefore, CACS does not allow the assessment of hemodynamic relevance of the calcified plaques or a possible microvascular disease. Presence and extent of CACS, therefore, rather represent a surrogate for the atherosclerotic plaque burden and does not give any information on the ischemic impact on the myocardium level. Thus, several studies tried to further improve the diagnosti
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