High-Risk Coronary Plaque on Computed Tomography Angiography: Time to Recognize a New Imaging Risk Factor.
High-Risk Coronary Plaque on Computed Tomography Angiography: Time to Recognize a New Imaging Risk Factor.
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计算机断层扫描血管造影中的高风险冠状动脉斑块:是时候识别新的成像风险因素了。
DOI:
10.1161/circimaging.117.007288
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发表时间:
2018
期刊:
影响因子:
--
通讯作者:
Hoffmann,Udo
中科院分区:
文献类型:
--
作者:
Ferencik,Maros;Hoffmann,Udo
2 Ferencik and Hoffmann High-Risk Plaque on CT: a New Imaging Risk Factor the strong association of significant obstructive CAD with MACE, the incremental prognostic value of high-risk plaque will be most prominent in patients with nonobstructive CAD. 9 To discuss the potential to modify medical therapy, it is helpful to put the probability of MACE in patients with highrisk plaque in the perspective of established treatment thresholds in primary prevention. As an example, Motoyama et al13 reported MACE rates of 0.6% in the absence of CAD, 1.2% for nonobstructive CAD without high-risk plaque, and 14.9% in patients with high-risk plaque and no stenosis for 4 years of follow-up. Thus, 10-year risk of events would be above 7.5%, an accepted threshold for the initiation of lipid-lowering therapies in patients with high-risk plaque even in the absence of obstructive CAD. However, the finding of high-risk plaque is not included in the current guidelines for lipid-lowering and antiplatelet treatment in secondary prevention. 14 The secondary prevention is recommended for patients with clinical atherosclerotic cardiovascular disease (defined as history of myocardial infarction, stable or unstable angina, coronary or other arterial revascularization, stroke, transient ischemic attack, or peripheral arterial disease presumed to be of atherosclerotic origin). The mere presence of coronary atherosclerotic plaque is not included in the list of diagnoses requiring secondary prevention. The primary prevention guidelines only recommend the use of coronary artery calcium≥ 300 as an additional factor guiding decision about the initiation of statin. 14 However, there are no clear guidelines for how indication of lipid-lowering therapies may be revised based on the presence and extent of CAD on coronary CTA. Nevertheless, there are already data demonstrating that incorporation of information on the presence and extent of CAD into the pooled cohort equation of the Atherosclerotic Cardiovascular Disease calculator significantly improves adequate allocation of statin therapy in nonobstructive CAD. 15, 16 Clearly, these data emphasize that the lack of guidelines directing the use of the preventative optimal medical therapy in patients with nonobstructive CAD remains a missed opportunity. Therapeutic uncertainty is reflected in large variations in the use of optimal medical therapies in patients with nonobstructive CAD. Only 47% of patients with nonobstructive CAD detected by invasive coronary angiography were receiving optimal medical therapy within 1 year. 17 Importantly, there was 2-fold variation in optimal medical therapy across hospitals. As it was shown in an analysis of the SCOT-HEART trial (Scottish Computed Tomography of the HEART Trial), the increase in preventative therapies (12-fold increase in aspirin use and 3.5-fold increase in statin use), predominantly in patients with nonobstructive CAD, resulted in 50% reduction in fatal and nonfatal myocardial infarctions. 18 Whether high-risk plaque, which has even stronger association with MACE as compared with the presence of any plaque, has also value in guiding the modification of preventative treatments is unknown. Data from longitudinal studies showed that intensive statin treatment could change the plaque progression and change plaque characteristics by increasing the volume of dense calcified plaque, potentially leading to plaque stabilization and decreasing high-risk plaque characteristics. 19 However, results from randomized clinical trials clearly demonstrating the benefit of preventative treatments in patients with high-risk plaque are missing. The community of clinical trials and imaging researchers should …
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影响因子:
5.3
作者:
Auscher, Soren;Heinsen, Laurits;Egstrup, Kenneth
通讯作者:
Egstrup, Kenneth
影响因子:
24
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Williams MC;Hunter A;Shah ASV;Assi V;Lewis S;Smith J;Berry C;Boon NA;Clark E;Flather M;Forbes J;McLean S;Roditi G;van Beek EJR;Timmis AD;Newby DE;SCOT-HEART Investigators
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SCOT-HEART Investigators
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通讯作者:
Ferencik, Maros
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5.4
作者:
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通讯作者:
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