Coronary artery calcium scoring: an evidence-based guide for primary care physicians.

Primary care physicians often must decide whether statin therapy would be appropriate (in addition to lifestyle modification) for managing asymptomatic individuals with borderline or intermediate risk for developing atherosclerotic cardiovascular disease (ASCVD), as assessed on the basis of traditional risk factors. In appropriate subjects, a simple, noninvasive measurement of coronary artery calcium can help clarify risk. Coronary atherosclerosis is a chronic inflammatory disease, with atherosclerotic plaque formation involving intimal inflammation and repeated cycles of erosion and fibrosis, healing and calcification. Atherosclerotic plaque formation represents the prognostic link between risk factors and future clinical events. The presence of coronary artery calcification is almost exclusively an indication of coronary artery disease, except in certain metabolic conditions. Coronary artery calcification can be detected and quantified in a matter of seconds by noncontrast electrocardiogram-gated low-dose X-ray computed tomography (coronary artery calcium scoring [CACS]). Since the publication of the seminal work by Dr. Arthur Agatston in 1990, a wealth of CACS-based prognostic data has been reported. In addition, recent guidelines from various professional societies conclude that CACS may be considered as a tool for reclassifying risk for atherosclerotic cardiovascular disease in patients otherwise assessed to have intermediate risk, so as to more accurately inform decisions about possible statin therapy in addition to lifestyle modification as primary preventive therapy. In this review, we provide an overview of CACS, from acquisition to interpretation, and summarize the scientific evidence for and the appropriate use of CACS as put forth in current clinical guidelines.

Non-contrast computed tomography is comparable to contrast-enhanced computed tomography for aortic volume analysis after endovascular abdominal aortic aneurysm repair.

OBJECTIVES: To evaluate whether non-contrast computed tomography (NCCT) images are as reliable as contrast-enhanced computed tomography (CECT) images for the measurement of aortic volume (AV). MATERIALS AND METHODS: A total of 316 pairs of AVs were retrospectively measured from 316 consecutive patients, who underwent endovascular aneurysm repair (EVAR). A standardised multidetector computed tomography protocol was used to obtain precontrast, arterial and delay-phase images. A single blinded, experienced observer measured the AV from the lowest renal artery to the aortic bifurcation by means of the disc-summation method, using the precontrast and arterial-phase images. A second blinded observer measured the AV again in 16 randomly chosen cases. RESULTS: Both NCCT and CECT yielded similar AVs that were highly correlated (r(2) = 0.99; P < 0.0001). Bland and Altman analysis revealed a small bias (mean ± 2 standard deviations: -0.9 ± 8 ml). The intraclass correlation coefficients (all >0.99; P < 0.0001) and low repeatability coefficients indicated that the AVs were reproducible with both methods. CONCLUSIONS: The AVs measured from NCCT images were accurate and highly reproducible compared with those from CECT images. Therefore, NCCT can be a reasonable alternative to CECT for AV assessment after EVAR. This is particularly important for patients with renal insufficiency (potentially sparing them from nephrotoxic contrast agents and unnecessary radiation) or allergy to contrast agents.

The utility of delayed-enhancement magnetic resonance imaging for identifying nonischemic myocardial fibrosis in asymptomatic patients with biopsy-proven systemic sarcoidosis.

BACKGROUND: The pathophysiology of sarcoidosis includes infiltrative inflammatory injury, as well as interstitial fibrosis formation. Delayed-enhancement (DE) magnetic resonance imaging (MRI) techniques have been shown to identify fibrotic tissue as areas of hyperenhancement. To test the hypothesis that DE-MRI can be used to identify myocardial fibrosis resulting from cardiac sarcoidosis, we assessed this method in asymptomatic patients with biopsy-proven systemic sarcoidosis. METHODS: Thirty-one patients with biopsy-confirmed systemic sarcoidosis and no known history of heart disease or sarcoid cardiac involvement underwent DE-MRI after gadolinium-chelate administration. The location and extent of DE were quantified by 2 radiologists experienced at evaluating cardiovascular MRI images. RESULTS: According to DE-MRI, 8 (26%) of the 31 patients had nonischemic fibrosis, as evidenced by abnormal DE patterns. Unlike characteristic ischemic injuries, most of the fibrosis was mid-myocardial, extending to the adjacent endocardium, epicardium, or both. The most frequent site of fibrosis was the basal inferoseptum, followed by the basal inferolateral wall. CONCLUSIONS: In asymptomatic patients with systemic sarcoidosis, DE-MRI may provide a novel, noninvasive method for the early identification of myocardial fibrosis.