Purpose: In aortic stenosis patients referred for surgical and transcatheter aortic valve replacement (AVR), the evidence of diagnostic accuracy of coronary computed tomography angiography (CCTA) has been limited. The objective of this study was to investigate the diagnostic accuracy of CCTA for significant coronary artery disease (CAD) in patients referred for AVR using invasive coronary angiography (ICA) as the gold standard. Materials and Methods: We searched databases for all diagnostic studies of CCTA in patients referred for AVR, which reported diagnostic testing characteristics on patient-based analysis required to pool summary sensitivity, specificity, positive-likelihood ratio, and negative-likelihood ratio. Significant CAD in both CCTA and ICA was defined by >50% stenosis in any coronary artery, coronary stent, or bypass graft. Results: Thirteen studies evaluated 1498 patients (mean age, 74 y; 47% men; 76% transcatheter AVR). The pooled prevalence of significant stenosis determined by ICA was 43%. Hierarchical summary receiver-operating characteristic analysis demonstrated a summary area under curve of 0.96. The pooled sensitivity, specificity, and positive-likelihood and negative-likelihood ratios of CCTA in identifying significant stenosis determined by ICA were 95%, 79%, 4.48, and 0.06, respectively. In subgroup analysis, the diagnostic profiles of CCTA were comparable between surgical and transcatheter AVR. Conclusions: Despite the higher prevalence of significant CAD in patients with aortic stenosis than with other valvular heart diseases, our meta-analysis has shown that CCTA has a suitable diagnostic accuracy profile as a gatekeeper test for ICA. Our study illustrates a need for further study of the potential role of CCTA in preoperative planning for AVR.
Effects of Sleep Deprivation on Neural Circulatory Control
Abstract —Effects of sleep deprivation on neural cardiovascular control may have important clinical implications. We tested the hypothesis that sleep deprivation increases heart rate, blood pressure, and sympathetic activity and potentiates their responses to stressful stimuli. We studied 8 healthy subjects (aged 40±5 years, 6 men and 2 women). Blood pressure, heart rate, forearm vascular resistance, and muscle sympathetic nerve activity were measured at rest and during 4 stressors (sustained handgrip, maximal forearm ischemia, mental stress, and cold pressor test). Measurements were obtained twice, once after normal sleep and once after a night of sleep deprivation. All measurements were obtained in a blinded, randomized manner. In comparison with normal sleep, sleep deprivation resulted in an increase in blood pressure (normal sleep versus sleep deprivation=82±8 versus 86±7 mm Hg, mean±SEM, P =0.012) and a decrease in muscle sympathetic nerve activity (normal sleep versus sleep deprivation=28±6 versus 22±6 bursts/min, P =0.017). Heart rate, forearm vascular resistance, and plasma catecholamines were not significantly changed by sleep deprivation, nor did sleep deprivation affect autonomic and hemodynamic responses to stressful stimuli. Sleep deprivation results in increased resting blood pressure, decreased muscle sympathetic nerve activity, and no change in heart rate. Thus, the pressor response to sleep deprivation is not mediated by muscle sympathetic vasoconstriction or tachycardia.