Objectives: This study sought to investigate the performance of various cardiac computed tomography (CT)-derived atherosclerotic plaque metrics for predicting provocable myocardial ischemia.
Background: The association of coronary arterial diameter stenosis with myocardial ischemia is only modest, but cardiac CT provides several other, readily available atherosclerosis metrics, which may have incremental value.
Methods: The study analyzed 873 nonstented coronary arteries and their myocardial perfusion territories in 356 patients (mean 62 years of age) enrolled in the CORE320 (Coronary Artery Evaluation using 320-row Multidetector Computed Tomography Angiography and Myocardial Perfusion) study. Myocardial perfusion defects in static CT perfusion imaging were graded at rest and after adenosine in 13 myocardial segments using a 4-point scale. The summed difference score was calculated by subtracting the summed rest score from the summed stress score. Reversible ischemia was defined as summed difference score ≥1. In a sensitivity analysis, results were also provided using single-photon emission computed tomography (SPECT) as the reference standard. Vessel based predictor variables included maximum percent diameter stenosis, lesion length, coronary calcium score, maximum cross-sectional calcium arc, percent atheroma volume (PAV), low-attenuation atheroma volume, positive (external) vascular remodeling, and subjective impression of "vulnerable plaque." The study used logistic regression models to assess the association of plaque metrics with myocardial ischemia.
Results: In univariate analysis, all plaque metrics were associated with reversible ischemia. In the adjusted logistic model, only maximum percent diameter stenosis (1.26; 95% confidence interval: 1.15 to 1.38) remained an independent predictor. With SPECT as outcome variable, PAV and "vulnerable" plaque remained predictive after adjustment. In vessels with intermediate stenosis (40% to 70%), no single metric had clinically meaningful incremental value.
Conclusions: Various plaque metrics obtained by cardiac CT predict provocable myocardial ischemia by CT perfusion imaging through their association with maximum percent stenosis, while none had significant incremental value. With SPECT as reference standard, PAV and "vulnerable plaque" remained predictors of ischemia after adjustment but the predictive value added to stenosis assessment alone was small.
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http://dx.doi.org/10.1016/j.jcmg.2018.05.019 | DOI Listing |
Cortex
January 2025
School of Psychology, Liverpool John Moores University, United Kingdom.
Background: Alzheimer's disease (AD) can be diagnosed by in vivo abnormalities of amyloid-β plaques (A) and tau accumulation (T) biomarkers. Previous studies have shown that analyses of serial position performance in episodic memory tests, and especially, delayed primacy, are associated with AD pathology even in individuals who are cognitively unimpaired. The earliest signs of cortical tau pathology are observed in medial temporal lobe (MTL) regions, yet it is unknown if serial position markers are also associated with early tau load in these regions.
View Article and Find Full Text PDFNat Rev Neurol
January 2025
J. Philip Kistler Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Three monoclonal antibodies directed against specific forms of the amyloid-β (Aβ) peptide have been granted accelerated or traditional approval by the FDA as treatments for Alzheimer disease, representing the first step towards bringing disease-modifying treatments for this disease into clinical practice. Here, we review the detection, underlying pathophysiological mechanisms and clinical implications of amyloid-related imaging abnormalities (ARIA), the most impactful adverse effect of anti-Aβ immunotherapy. ARIA appears as regions of oedema or effusions (ARIA-E) in brain parenchyma or sulci or as haemorrhagic lesions (ARIA-H) in the form of cerebral microbleeds, convexity subarachnoid haemorrhage, cortical superficial siderosis or intracerebral haemorrhage.
View Article and Find Full Text PDFCardiovasc Diagn Ther
December 2024
Department of Cardiology, Beijing An Zhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Engineering Research Center of Cardiovascular Wisdom Diagnosis and Treatment, Beijing, China.
Background: The prevalence of very high-risk atherosclerotic cardiovascular disease (ASCVD) is significant in China, with suboptimal rates of low-density lipoprotein cholesterol (LDL-C) compliance exacerbating plaque instability and causing a higher incidence of major adverse cardiac events (MACEs). Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) are effective in reducing LDL-C levels, increase the stability of vulnerable plaque, and influence the progression of atherosclerosis through multiple mechanisms as demonstrated in animal studies. However, there is currently a lack of evidence regarding the efficacy and safety of high-intensity statin therapy combined with PCSK9i in the secondary prevention of ASCVD in the Chinese population.
View Article and Find Full Text PDFTheranostics
January 2025
Joint Department of Biomedical Engineering, University of North Carolina at Chapel Hill and North Carolina State University, Chapel Hill, NC, 27599, USA.
Alzheimer's Disease (AD) is the most common form of dementia and one of the leading causes of death. AD is known to be correlated to tortuosity in the microvasculature as well as decreases in blood flow throughout the brain. However, the mechanisms behind these changes and their causal relation to AD are poorly understood.
View Article and Find Full Text PDFmedRxiv
December 2024
Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA.
The Circle of Willis (CW) is a critical cerebrovascular structure that supports collateral blood flow to maintain brain perfusion and compensate for eventual occlusions. Increased tortuosity of high-risk vessels within the CW has been implicated as a marker in the progression of cerebrovascular diseases especially in structures like the internal carotid artery (ICA). This is partly due to age-related plaque deposition or arterial stiffening.
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