Accuracy of IVUS-Based Machine Learning Segmentation Assessment of Coronary Artery Dimensions and Balloon Sizing.

Background: Accurate intravascular ultrasound (IVUS) measurements are important in IVUS-guided percutaneous coronary intervention optimization by choosing the appropriate device size and confirming stent expansion. Objectives: The purpose of this study was to assess the accuracy of machine learning (ML) automatic segmentation of coronary artery vessel and lumen dimensions and balloon sizing. Methods: Using expert analysis as the gold standard, ML segmentation of 60 MHz IVUS images was developed using 8,076 IVUS cross-sectional images from 234 patients, which were randomly split into training (83%) and validation (17%) data sets. The performance of ML segmentation was then evaluated using an independent test data set (437 images from 92 patients). The endpoints were the agreement rate between ML vs experts' measurements for appropriate balloon size selection, and lumen and acute stent areas. Appropriate balloon size was determined by rounding down from the mean vessel diameter or rounding up from the mean lumen diameter to the next balloon size. The difference of lumen area ≥0.5 mm2 was considered as clinically significant. Results: ML model segmentation correlated well with experts' segmentation for training data set with a correlation coefficient of 0.992 and 0.993 for lumen and vessel areas, respectively. The agreement rate in lumen and acute stent areas was 85.5% and 97.0%, respectively. The agreement rate for appropriate balloon size selection was 70.6% by vessel diameter only and 92.4% by adding lumen diameter. Conclusions: ML model IVUS segmentation measurements were well-correlated with those of experts and selected an appropriate balloon size in more than 90% of images.

Case Report: Invasive and Non-invasive Hemodynamic Assessment of Coronary Artery Disease: Strengths and Weaknesses.

Coronary angiography has been the gold standard for assessment of coronary artery disease (CAD) and guidance for percutaneous coronary interventions (PCI). Physiology-guided PCI has shown increased safety and efficacy, improved resource utilization, and better clinical outcomes in patients with stable angina and acute coronary syndromes. The three cases presented and discussed in this report illustrate the strengths and weaknesses of the available invasive and non-invasive methods for the physiological assessment of CAD. As technology evolves, invasive non-wire-based (angiography-derived FFR) and non-invasive (FFRCT) modalities for the hemodynamic assessment of CAD appear to provide reliable and user-friendly alternatives to the gold standard invasive wire-based techniques. Interventional cardiologists and cardiovascular healthcare providers should be familiar with the strengths and weaknesses of the available hemodynamic assessment modalities.

Role of Invasive Functional Assessment in Surgical Revascularization of Coronary Artery Disease.

In patients with stable coronary artery disease, percutaneous coronary intervention is associated with improved outcomes if the lesion is deemed significant by invasive functional assessment using fractional flow reserve. Recent studies have shown that a revascularization strategy using instantaneous wave-free ratio is noninferior to fractional flow reserve in patients with intermediate-grade stenoses. The decision to perform coronary artery bypass grafting surgery is usually based on anatomic assessment of stenosis severity by coronary angiography. The data on the role of invasive functional assessment in guiding surgical revascularization are limited. In this review, we discuss the diagnostic and prognostic significance of invasive functional assessment in patients considered for coronary artery bypass grafting. In addition, we critically discuss ongoing and future clinical trials on the role of invasive functional assessment in surgical revascularization.

Assessment of endothelial shear stress in patients with mild or intermediate coronary stenoses using coronary computed tomography angiography: comparison with invasive coronary angiography.

Characterization of endothelial shear stress (ESS) may allow for prediction of the progression of atherosclerosis. The aim of this investigation was to develop a non-invasive approach for in vivo assessment of ESS by coronary computed tomography angiography (CTA) and to compare it with ESS derived from invasive coronary angiography (ICA). A total of 41 patients with mild or intermediate coronary stenoses who underwent both CTA and ICA were included in the analysis. Two geometrical models of the interrogated vessels were reconstructed separately from CTA and ICA images. Subsequently, computational fluid dynamics were applied to calculate the ESS, from which ESSCTA and ESSICA were derived, respectively. Comparisons between ESSCTA and ESSICA were performed on 163 segments of 57 vessels in the CTA and ICA models. ESSCTA and ESSICA were similar: mean ESS: 4.97 (4.37-5.57) Pascal versus 4.86 (4.27-5.44) Pascal, p = 0.58; minimal ESS: 0.86 (0.67-1.05) Pascal versus 0.79 (0.63-0.95) Pascal, p = 0.37; and maximal ESS: 14.50 (12.62-16.38) Pascal versus 13.76 (11.44-16.08) Pascal, p = 0.44. Good correlations between the ESSCTA and the ESSICA were observed for the mean (r = 0.75, p < 0.001), minimal (r = 0.61, p < 0.001), and maximal (r = 0.62, p < 0.001) ESS values. In conclusion, geometrical reconstruction by CTA yields similar results to ICA in terms of segment-based ESS calculation in patients with low and intermediate stenoses. Thus, it has the potential of allowing combined local hemodynamic and plaque morphologic information for risk stratification in patients with coronary artery disease.

Combined non-invasive assessment of endothelial shear stress and molecular imaging of inflammation for the prediction of inflamed plaque in hyperlipidaemic rabbit aortas.

AIMS: To evaluate the incremental value of low endothelial shear stress (ESS) combined with high-resolution magnetic resonance imaging (MRI)- and computed tomography angiography (CTA)-based imaging for the prediction of inflamed plaque. METHODS AND RESULTS: Twelve hereditary hyperlipidaemic rabbits underwent quantitative analysis of plaque in the thoracic aorta with 256-slice CTA and USPIO-enhanced (ultra-small superparamagnetic nanoparticles, P904) 1.5-T MRI at baseline and at 6-month follow-up. Computational fluid dynamics using CTA-based 3D reconstruction of thoracic aortas identified the ESS patterns in the convex and concave curvature subsegments of interest. Subsegments with low baseline ESS exhibited significant increase in wall thickness and plaque inflammation by MRI, in non-calcified plaque burden by CTA, and developed increased plaque size, lipid and inflammatory cell accumulation (high-risk plaque features) at follow-up by histopathology. Multiple regression analysis identified baseline ESS and inflammation by MRI to be independent predictors of plaque progression, while receiver operating curve analysis revealed baseline ESS alone or in combination with inflammation by MRI as the strongest predictor for augmented plaque burden and inflammation (low ESS at baseline: AUC = 0.84, P < 0.001; low ESS and inflammation by molecular MRI at baseline: AUC = 0.89, P < 0.001). CONCLUSION: Low ESS predicts progression of plaque burden and inflammation as assessed by non-invasive USPIO-enhanced MRI. Combined non-invasive assessment of ESS and imaging of inflammation may serve to predict plaque with high-risk features.

In-vivo assessment of the natural history of coronary atherosclerosis: vascular remodeling and endothelial shear stress determine the complexity of atherosclerotic disease progression.

PURPOSE OF REVIEW: Atherosclerotic disease progression is determined by localized plaque growth, which is induced by systemic and local hemodynamic factors, and the nature of the wall remodeling response. The purpose of this review is to summarize the processes underlying the heterogeneity of coronary atherosclerosis progression in relation to the local hemodynamic and arterial remodeling environment. RECENT FINDINGS: Multiple competing biological processes in the extracellular matrix define the extent of vascular remodeling and disease progression. The remodeling phenomenon is not consistent but is characterized by great phenotypical heterogeneity which reflects the complex effect of systemic, genetic and hemodynamic factors on the arterial wall response to plaque formation and progression. The exaggeration of expansive remodeling (i.e., excessive expansive remodeling) likely contributes to the transformation of an initially favorable action into an excessive course of vessel expansion, continued disease progression and plaque instability. Extremely low endothelial shear stress and excessive expansive remodeling establish a vicious cycle which leads to the formation of severe plaques with high-risk characteristics. SUMMARY: The dynamic interplay between the local hemodynamic environment and the wall remodeling behavior determines the complexity of the natural history of atherosclerosis and explains the development of localized plaque vulnerability.

Risk factors and drug interactions predisposing to statin-induced myopathy: implications for risk assessment, prevention and treatment.

HMG-CoA reductase inhibitors ('statins') represent the most effective and widely prescribed drugs currently available for the reduction of low-density lipoprotein cholesterol, a critical therapeutic target for primary and secondary prevention of cardiovascular atherosclerotic disease. In the face of the established lipid lowering and the emerging pleiotropic properties of statins, the patient population suitable for long-term statin treatment is expected to further expand. An overall positive safety and tolerability profile of statins has been established, although adverse events have been reported. Skeletal muscle-related events are the most common adverse events of statin treatment. Statin-induced myopathy can (rarely) manifest with severe and potentially fatal cases of rhabdomyolysis, thus rendering the identification of the underlying predisposing factors critical. The purpose of this review is to summarize the factors that increase the risk of statin-related myopathy. Data from published clinical trials, meta-analyses, postmarketing studies, spontaneous report systems and case reports for rare effects were reviewed. Briefly, the epidemiology, clinical spectrum and molecular mechanisms of statin-associated myopathy are discussed. We further analyse in detail the risk factors that precipitate or increase the likelihood of statin-related myopathy. Individual demographic features, genetic factors and co-morbidities that may account for the significant interindividual variability in the myopathic risk are presented. Physicochemical properties of statins have been implicated in the differential risk of currently marketed statins. Pharmacokinetic interactions with concomitant medications that interfere with statin metabolism and alter their systemic bioavailability are reviewed. Of particular clinical interest in cases of resistant dyslipidaemia is the interaction of statins with other classes of lipid-lowering agents; current data on the relative safety of available combinations are summarized. Finally, we provide an update of current guidelines for the prevention and management of statin myopathy. The identification of patients with an increased proclivity to statin-induced myopathy could allow more cost-effective approaches of monitoring and screening, facilitate targeted prevention of potential complications, and further improve the already overwhelmingly positive benefit-risk ratio of statins.