Coronary artery disease
Comparison of the Relation Between the Calcium Score and Plaque Characteristics in Patients With Acute Coronary Syndrome Versus Patients With Stable Coronary Artery Disease, Assessed by Computed Tomography Angiography and Virtual Histology Intravascular Ultrasound

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A considerable number of patients with an acute coronary syndrome (ACS) who present with a 0 or low calcium score (CS) still demonstrate coronary artery disease (CAD) and significant stenosis. The aim of the present study was to evaluate the relation between the CS and the degree and character of atherosclerosis in patients with suspected ACS versus patients with stable CAD obtained by computed tomography angiography and virtual histology intravascular ultrasound (VH IVUS). Overall 112 patients were studied, 53 with ACS and 59 with stable CAD. Calcium scoring and computed tomography angiography were performed and followed by VH IVUS. On computed tomography angiography each segment was evaluated for plaque and classified as noncalcified, mixed, or calcified. Vulnerable plaque characteristics on VH IVUS were defined by percent necrotic core and presence of thin-cap fibroatheroma. If the CS was 0, patients with ACS had a higher mean number of plaques (5.0 ± 2.0 vs 2.0 ± 1.9, p <0.05) and noncalcified plaques (4.6 ± 3.5 vs 1.3 ± 1.9, p <0.05) on computed tomography angiography than those with stable CAD. If the CS was 0, VH IVUS demonstrated that patients with ACS had a larger amount of necrotic core area (0.58 ± 0.73 vs 0.22 ± 0.43 mm2, p <0.05) and a higher mean number of thin-cap fibroatheromas (0.6 ± 0.7 vs 0.1 ± 0.3, p <0.05) than patients with stable CAD. In conclusion, even in the presence of a 0 CS, patients with ACS have increased plaque burden and increased vulnerability compared to patients with stable CAD. Therefore, absence of coronary calcification does not exclude the presence of clinically relevant and potentially vulnerable atherosclerotic plaque burden in patients with ACS.

Section snippets

Methods

The study population consisted of 112 patients without known CAD (defined as previous myocardial infarction, coronary arterial bypass grafting, and percutaneous coronary intervention) who were referred for CTA for noninvasive evaluation of chest pain. Subsequently patients were referred for invasive coronary angiography in combination with VH IVUS based on a patient's clinical presentation and/or imaging results. Patient data were prospectively collected in the departmental cardiology

Results

Overall 112 patients were studied; 53 patients presented with ACS and 59 presented with stable CAD. No differences were observed in the prevalence of risk factors for CAD between the 2 groups (Table 1). In patients with ACS cardiac troponin levels were increased in 11 patients (21%), and in 31 patients (58%) significant CAD was demonstrated on invasive coronary angiography. VH IVUS could be performed in all patients and was obtained in 241 vessels (124 vessels [51%] in ACS and 117 vessels [48%]

Discussion

The main finding of the present study was that clinical presentation (ACS vs stable CAD) has a strong impact on the relation between the CS and coronary plaque characteristics. Although the mean number of plaques was similar between patients with ACS and those with stable CAD, when coronary calcium was absent, the plaque burden on computed tomography angiography was significantly greater in patients with ACS than in patients with stable CAD. Invasive VH IVUS findings paralleled noninvasive

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This work was supported by Grant 2007B223 from the Dutch Heart Foundation, The Hague, The Netherlands to Dr. van Velzen; the Dutch Technology Foundation STW, Utrecht, The Netherlands; and Grant 10084 from Applied Science Division I and the Technology Program of the Ministry of Economic Affairs, The Hague, The Netherlands to Dr. de Graaf. Dr. Jukema receives grants from Biotronik, Berlin, Germany; Boston Scientific, Natick; Astra Zeneca, London, United Kingdom; Pfizer, New York; MSD, New Jersey. Dr. Schalij has research grants from Biotronik, Berlin, Germany; Boston Scientific, Natick, Massachusetts; and Medtronic, Minneapolis, Minnesota. Dr. Bax has research grants from Biotronik; BMS Medical Imaging, North Billerica, Massachusetts; Boston Scientific; Edwards Lifesciences, Irvine, California; GE Healthcare, Buckinghamshire, United Kingdom; Medtronic; and St. Jude Medical, St. Paul, Minnesota.

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