Hepatosteatosis and Atherosclerotic Plaque at Coronary CT Angiography.

Purpose: To assess the association between nonalcoholic fatty liver disease (NAFLD) and quantitative atherosclerotic plaque at CT. Materials and Methods: In this post hoc analysis of the prospective Scottish Computed Tomography of the HEART trial (November 2010 to September 2014), hepatosteatosis and coronary artery calcium score were measured at noncontrast CT. Presence of stenoses, visually assessed high-risk plaque, and quantitative plaque burden were assessed at coronary CT angiography. Multivariable models were constructed to assess the impact of hepatosteatosis and cardiovascular risk factors on coronary artery disease. Results: Images from 1726 participants (mean age, 58 years ± 9 [SD]; 974 men) were included. Participants with hepatosteatosis (155 of 1726, 9%) had a higher body mass index, more hypertension and diabetes mellitus, and higher cardiovascular risk scores (P < .001 for all) compared with those without hepatosteatosis. They had increased coronary artery calcium scores (median, 43 Agatston units [AU] [interquartile range, 0-273] vs 19 AU [0-225], P = .046), more nonobstructive disease (48% vs 37%, P = .02), and higher low-attenuation plaque burden (5.11% [0-7.16] vs 4.07% [0-6.84], P = .04). However, these associations were not independent of cardiovascular risk factors. Over a median of 4.7 years, there was no evidence of a difference in myocardial infarction between those with and without hepatosteatosis (1.9% vs 2.4%, P = .92). Conclusion: Hepatosteatosis at CT was associated with an increased prevalence of coronary artery disease at CT, but this was not independent of the presence of cardiovascular risk factors.Keywords: CT, Cardiac, Nonalcoholic Fatty Liver Disease, Coronary Artery Disease, Hepatosteatosis, Plaque QuantificationClinical trial registration no. NCT01149590 Supplemental material is available for this article. © RSNA, 2022See also commentary by Abohashem and Blankstein in this issue.

Latest Advances in Cardiac CT.

Recent rapid technological advancements in cardiac CT have improved image quality and reduced radiation exposure to patients. Furthermore, key insights from large cohort trials have helped delineate cardiovascular disease risk as a function of overall coronary plaque burden and the morphological appearance of individual plaques. The advent of CT-derived fractional flow reserve promises to establish an anatomical and functional test within one modality. Recent data examining the short-term impact of CT-derived fractional flow reserve on downstream care and clinical outcomes have been published. In addition, machine learning is a concept that is being increasingly applied to diagnostic medicine. Over the coming decade, machine learning will begin to be integrated into cardiac CT, and will potentially make a tangible difference to how this modality evolves. The authors have performed an extensive literature review and comprehensive analysis of the recent advances in cardiac CT. They review how recent advances currently impact on clinical care and potential future directions for this imaging modality.

Substantial and Sustained Improvements in Blood Pressure, Weight and Lipid Profiles from a Carbohydrate Restricted Diet: An Observational Study of Insulin Resistant Patients in Primary Care.

Hypertension is the second biggest known global risk factor for disease after poor diet; perhaps lifestyle interventions are underutilized? In a previous small pilot study, it was found that a low carbohydrate diet was associated with significant improvements in blood pressure, weight, 'deprescribing' of medications and lipid profiles. We were interested to investigate if these results would be replicated in a larger study based in 'real world' GP practice. 154 patients with type 2 diabetes or impaired glucose tolerance were recruited into an observational cohort study in primary care. The effects of a low carbohydrate diet sustained for an average of two years (interquartile range 10-32 months) on cardiovascular risk factors were examined. Results demonstrate significant and substantial reductions in blood pressure (mean reduction of systolic BP 10.9 mmHg (interquartile range 0-22 mmHg) (p < 0.0001), mean reduction in diastolic BP 6.3 mmHg (interquartile range 0-12.8 mmHg) (p < 0.0001) and mean weight reduction of 9.5 Kg (interquartile range 5-13 Kg) (p < 0.0001) together with marked improvement in lipid profiles. This occurred despite a 20% reduction in anti-hypertensive medications. This novel and potentially highly effective dietary modification, done very cheaply alongside routine care, offers hope that should be tested in a large prospective trial.

Evading the fate of Pheidippides: acute coronary thrombosis in a young marathon runner with minimal atherosclerosis but sickle cell trait.

Marathon running transiently increases the risk of sudden cardiac death. Some previous studies have suggested that this is due to relatively advanced but asymptomatic atherosclerosis. Other theories suggest that potentiation of inflammation and the coagulation cascade, by extremes of exertion, is more important. We present a clinical case of a young, previously fit athlete who felt chest discomfort eight miles into a marathon but finished the race. Shortly after completion he felt very unwell and had chest pain. Ambulance electrocardiograms showed evidence of an evolving anterior myocardial infarction. Invasive assessment with coronary angiography and intravascular ultrasound was able to show the mechanism of thrombosis. Fissuring of a small rim of atherosclerosis potentiated a large pro-thrombotic response, the patient was also found to have sickle cell trait. Medical treatment with blood thinning drugs was able to restore normality to the vessel over a period of two weeks, without the need for angioplasty or stent implantation.

Site-specific intravascular ultrasound analysis of remodelling index and calcified necrosis patterns reveals novel blueprints for coronary plaque instability.

AIMS: Post-mortem pathological studies have shown that a "vulnerable" plaque is the dominant patho-physiological mechanism responsible for acute coronary syndromes (ACS). One way to improve our understanding of these plaques in vivo is by using histological "surrogates" created by intravascular ultrasound derived virtual histology (IVUS-VH). Our aim in this analysis was to determine the relationship between site-specific differences in individual plaque areas between ACS plaques and stable plaques (SP), with a focus on remodelling index and the pattern of calcifying necrosis. METHODS AND RESULTS: IVUS-VH was performed before percutaneous intervention in both ACS culprit plaques (CP) n=70 and stable disease (SP) n=35. A total of 210 plaque sites were examined in 105 lesions at the minimum lumen area (MLA) and the maximum necrotic core site (MAX NC). Each plaque site had multiple measurements made including some novel calculations to ascertain the plaque calcification equipoise (PCE) and the calcified interface area (CIA). CP has greater amounts of positive remodelling at the MLA (RI@MLA): 1.1 (±0.17) vs. 0.95 (±0.14) (P<0.001); lower values for PCE 30% vs. 54% (P<0.001) but a higher CIA 5.38 (±2.72) vs. 3.58 (±2.26) (P=0.001). These features can provide discriminatory ability between plaque types with area under the curve (AUC) measurements between 0.65-0.86. The cut-off values with greatest sensitivity and specificity to discriminate CP morphologies were: RI @ MLA >1.12; RI @ MAX NC >1.22; PCE @ MLA <47.1%; PCE @MAX NC <47.3%; CIA @ MLA >2.6; CIA @ MAX NC >3.1. CONCLUSIONS: Determining the stage of calcifying necrosis, along with the remodelling index can discriminate between stable and ACS related plaques. These findings could be applied in the future to help detect plaques that have a vulnerable phenotype.

Double jeopardy: multi-modality imaging of monozygotic "twin cap" atherosclerosis.

The investigation of asymptomatic but potentially vulnerable atherosclerosis is not yet a major focus for clinical Cardiologists. We have illustrated the contemporary investigation and treatment of such disease using a clinical case that involved monozygotic twins. One twin (T1) had unfortunately suffered a cardiac arrest whilst jogging and survived only due to bystander CPR and prompt defibrillation. His identical twin brother (T2), on subsequent investigation, harbours a compositionally identical lesion in a proximal coronary vessel that has not yet ruptured or provoked a clinical event. Following the presentation of both non-invasive and invasive images, we discuss the need for active suspicion and intensive treatment for those people with a 'genetic' risk of future myocardial infarction.

Construction and validation of a plaque discrimination score from the anatomical and histological differences in coronary atherosclerosis: the Liverpool IVUS-V-HEART (Intra Vascular UltraSound-Virtual-Histology Evaluation of Atherosclerosis Requiring Treatment) study.

AIMS: New markers to help stratify coronary atherosclerosis are needed. Although attempts have been made to differentiate active lesions from those that are stable, none of these has ever been formalised into a discriminatory score. The aim of this study was to analyse the differences between culprit ACS lesions and culprit stable angina lesions with intravascular ultrasound-derived virtual histology and to construct and validate a plaque score. METHODS AND RESULTS: Prior to percutaneous coronary intervention (PCI), we performed volumetric, intravascular ultrasound-derived virtual histology (IVUS-VH) analysis in acute coronary syndrome (ACS) culprit lesions (AC - n=70) and stable angina culprit lesions (SC - n=35). A direct statistical comparison of IVUS-VH data and multiple logistic regression analysis was undertaken. Four main factors were found to be associated (p<0.05) with an AC lesion phenotype: necrotic core/dense calcium (NC/DC) ratio; minimum lumen area <4 mm2 (MLA <4); remodelling index @MLA >1.05 and VH-TCFA presence. Calculation of each logistic regression coefficient and the equation produces an active plaque discrimination score with an AUC of 0.96 on receiver operating characteristics (ROC) analysis. Validation of the score in 50 independent plaques from the Thoraxcenter in Rotterdam revealed an AUC of 0.71, confirming continued diagnostic ability. CONCLUSIONS: We have found four features on IVUS and VH that can predict and discriminate ACS culprit lesion phenotypes from those that are clinically stable. Subsequently, we have constructed and validated the Liverpool Active Plaque Score based upon these features. It is hoped this score may help diagnose active coronary plaques, in the future, to help prevent major adverse cardiac events.

Defining the magnitude of measurement variability in the virtual histology analysis of acute coronary syndrome plaques.

BACKGROUND: Previous intravascular ultrasound-based virtual histology (IVUS-VH) measurement variability studies have been confined to single-frame or short-segment analysis in stable patients with minimal disease. We sought to determine the magnitude of human measurement variability in acute coronary syndrome (ACS) plaques. METHODS AND RESULTS: Prior to percutaneous coronary intervention, we performed IVUS-VH analysis in troponin-positive ACS culprit lesions. A total of 3840 IVUS-VH frames were analysed by two operators to determine intra- and inter-observer variability. The plaque constituent area and volumes were compared using intra-class correlation coefficient (ICC); within-subjects standard deviation (WSSD, mm(2) or mm(3)) and the repeatability coefficient (RCO) to quantify the magnitude of operator error that 95% of future measurements should not exceed. The majority of intra- and inter-observer measurements had ICC of >0.92 confirming excellent agreement. Only the fibrous area (0.86), fibro-fatty (FF) area (0.72) and FF volume (0.87) had ICC levels suggesting an operator error >10%. However, the mean RCO and the percentage this represents in single-frame analysis (area error) varied across the plaque subtypes: fibrous area = 1.64 mm(2) (59%); FF area = 0.49 mm(2) (140%); necrotic core (NC) area = 0.39 mm(2) (21.3%); dense calcium (DC) area = 0.29 mm(2) (33.7%). For full lesion pullbacks (volume error): fibrous volume = 8.14 mm(3) (9.9%); FF volume = 5.63 mm(3) (53.8%); NC volume = 3.78 mm(3) (6.9%) and DC = 2.4 mm(3) (9.6%) CONCLUSION: As in previous studies, intra- and inter-observer ICC suggests good agreement between observers. However, this can still represent large measurement error values and percentages. These findings could impact on the interpretation of previous studies and influence future studies using IVUS-VH measurements as endpoints.

How should I treat a spontaneously reperfused acute STEMI that involves the left main stem and proximal LAD?

BACKGROUND: A 41-year-old female with 90 minutes of severe chest pain and ST-elevation in leads V1-V2 underwent emergency coronary angiography with a view to primary angioplasty. INVESTIGATIONS: Physical examination, electrocardiography, coronary angiography. DIAGNOSIS: ST-segment elevation anterior myocardial infarction. MANAGEMENT: Coronary angiography, antiplatelet and antithrombotic therapy, statin, angiotensin-converting enzyme inhibitor, beta blocker, IVUS and percutaneous coronary intervention (PCI)

Virtual histology imaging in acute coronary syndromes: useful or just a research tool?

Acute coronary syndromes (ACS) frequently cause considerable morbidity and mortality with a high risk of further events within the following year, despite the use of percutaneous coronary intervention (PCI). Numerous studies have described the concept of acute, partial or complete thrombotic occlusion of the coronary artery, which occurs at the site of a friable atherosclerotic plaque with a lipidrich necrotic core and a ruptured overlying thin fibrous cap ("culprit lesion"). Moreover, this process appears independent of the severity of the underlying stenosis. Most of our knowledge about the morphological characteristics of culprit lesions has been obtained from necropsy studies of lesions at the extreme end of the ACS spectrum. The development of intravascular ultrasound (IVUS) with virtual histology (VH), using spectral analysis of the radiofrequency ultrasound backscatter signals to identify the components of atherosclerotic plaque, has allowed in-vivo delineation of the relative contributions of necrotic core and fibrous atheroma in unstable lesions. This evidence suggests that there may be variations in the morphology of plaques that rupture and promote thrombosis in ACS, rather than the traditionally accepted view that a common pathological mechanism is at play. This imaging modality, therefore, provides great potential for invivo information about the culprit lesion. In this review article, we explore the background and potential application of virtual histology to improve the invasive treatment of ACS patients.