Coronary Vessel Wall Research Articles

Percutaneous coronary intervention in spontaneous coronary artery dissection: a case-control study

Abstract Background Spontaneous Coronary Artery Dissection (SCAD) is an important cause of acute coronary syndrome particularly in young-middle aged women. Revascularisation is challenging due to an underlying disrupted and friable coronary vessel wall leading to widely reported worse outcomes than for atherosclerotic coronary disease. Therefore, a conservative approach where possible is favoured however in some cases haemodynamic instability, ongoing ischaemia and reduced distal flow mandates consideration of revascularisation. Purpose To compare SCAD survivors managed with PCI or conservatively in terms of presentation characteristics, complications and long-term outcomes. Methodology and results 226 angiographically confirmed SCAD survivors (95% female,47±9.7yrs) who underwent PCI were compared in a case control study with two hundred and twenty-five angiographically confirmed SCAD survivors (92% female, 49±9.9yrs) who were conservatively managed. Patients were recruited from UK, Spanish and Dutch SCAD registries and both groups were well matched in terms of baseline demographics. Those treated with PCI were more likely to present with proximal SCAD (30.8% vs 7.6% P<0.01) and ST elevation myocardial infarction (STEMI) or cardiac arrest with reduced flow (32.3% vs 6.3% P<0.01). Intervention was performed with stents in 72.4%, plain old balloon angioplasty in 21.1% and wiring in 6.4% of cases and more often for multi-segment disease (40.8% vs 26.3% P<0.01). In cases with initial reduced flow undergoing PCI an improvement in flow was seen in 83%. Analysis of UK PCI cases (n=144) reveal complications in 56 (38.8%). However, when assessed for significance defined by a reduction in flow in a proximal/mid vessel, stent extension into left main stem, iatrogenic dissection requiring PCI and CABG as a consequence of PCI only 13 cases (9%) met criteria. Iatrogenic dissection accounts for the majority (76.9%). SCAD lesion length was associated with presence of complications (P=0.025). There was a non-significant trend towards major adverse cardiovascular events (MACE) occurring more frequently in those undergoing PCI (18% vs 11% P=0.067) driven by revascularisation (5% vs 1% P=0.036). Median follow up was 2.7 years. Conclusions PCI in SCAD is often performed in higher risk patients; in those presenting with reduced flow, the majority demonstrate improvement. Importantly whilst overall complication rates were similar to those widely reported, clinically significant complications were low. Multivariate modelling will reveal factors associated with complications to aid future decision making in this challenging patient group. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): British Heart Foundation

The involvement of protein TNFSF18 in promoting p-STAT1 phosphorylation to induce coronary microcirculation disturbance in atherosclerotic mouse model.

The inflammation of coronary endothelium was critically involved in the pathogenesis of atherosclerosis. The purpose of the study was to reveal the roles of TNFSF18 in promoting p-STAT1 phosphorylation to induce disturbance of coronary microcirculation in atherosclerotic mouse model. This study was dividedly transfected TNFSF18 inhibitor, small interfering-TNFSF18 plasmid (si-TNFSF18) and a blank vector plasmid into atherosclerotic mouse model. Results showed that the coronary vascular lumen was narrowed and crescent plaques were adhered to the coronary vessel wall in atherosclerotic mouse model. However, the accumulation of microthrombus in coronary artery and vascular crescent plaques were evidently reduced with the antagonistic TNFSF18. Besides, the inflammatory cytokines TNF-α, TNF-β and IL-1β were abundant in mouse model, and TNFSF18 inhibition decreased the secretion of cytokines. Meanwhile, the amount of Th1 cells were also reduced after transfected with TNFSF18 inhibitor and si-TNFSF18 plasmid compared with the mouse model transfected with blank vector plasmid. Moreover, the protein TNFSF18 was highly expressed in the cytoplasm and p-STAT1 was located in cell nucleus of the mouse model coronary vascular tissues. Consistently, the proteins TNFSF18, p-STAT1, VCAM1, ICAM1, ITGAD and ITGB3 were significantly expressed in atherosclerotic mouse model, while antagonistic TNFSF18, conversely, decreased the proteins' expression. Taken together, this study indicated that the coronary endothelial inflammation triggered TNFSF18 expression, which promoted p-STAT1 phosphorylation to activate the proteins VCAM1, ICAM1, ITGAD and ITGB3, thus exacerbating coronary microcirculation disorder in atherosclerotic mouse model.

Eosinophilic Granulomatosis with Polyangiitis with Pulmonary and Cardiac Involvement

A 62-year-old patient with bronchial asthma and chronic rhinosinusitis underwent inguinal hernia surgery. After the operation, sudden circulatory arrest occurred, requiring cardiopulmonary resuscitation. Coronary angiography revealed a 99 % proximal stenosis of right coronary artery (RCA) with unsuspicious and smooth coronary vessel walls. In the further course, several similar events occurred, but without pathological findings in the coronary angiography. Initially, echocardiography showed slightly reduced left ventricular ejection fraction of 45 %. Chest radiography revealed bilateral pulmonary infiltrates, and white blood cell count showed severe eosinophilia (37 %). Serological antibody testing including ANA, ENA and c-/p-ANCA was negative. Myeloproliferative pathologies were excluded by bone marrow puncture. The patient suffered from emerging dyspnea, weakness, and ongoing weight loss. A methylprednisolone pulse of 250 mg/d for 3 days remained without significant effect, so that the patient was eventually referred to our university hospital due to ongoing clinical deterioration. On admission, the patient suffered from weakness, progressive muscular atrophy, and dyspnea on exertion. Physical examination revealed a right-sided peroneal paralysis. Bronchial lavage detected severe eosinophil alveolitis (37 %), and laboratory findings showed elevated cardiac enzymes and NT-proBNP (Troponin-T > 700 ng/l, NT-proBNP > 10.000 ng/l). Echocardiography revealed a dramatic deterioration of cardiac function (LVEF 16 %). Interdisciplinary discussion between pulmonologists and cardiologists lead to the diagnosis of ANCA-negative eosinophilic granulomatosis with polyangiitis (EGPA) with pulmonary and cardiac involvement. Initiation of immunosuppressive therapy with methylprednisolone 1000 mg/d for 3 days followed by cyclophosphamide therapy (6 pulses, administered every 4 weeks) led to substantial symptomatic improvement, complete regression of pulmonary infiltrates and marked recovery of cardiac function (LVEF 47 %). CONCLUSION: Serological detection of elevated ANCAs is not necessary for diagnosis of EGPA. Only 30 - 70 % of patients are positive for these, particularly if neurological and/or renal rather than cardiac and/or pulmonary involvement is present. This may be a pitfall in establishing the correct diagnosis. Induction therapy with cyclophosphamide is the preferred treatment for steroid-refractory EGPA with life-threatening organ involvement.

Progress of quantitative intravascular optical coherence tomography

Intravascular optical coherence tomography (IVOCT) has emerged as a high-resolution and minimal-invasive imaging technique that provides high-speed visualization of coronary arterial vessel walls and clearly displays the vessel lumen and lesions under the intima. However, morphological gray-scale images cannot provide enough information about the tissue components to accurately characterize the plaque tissues including calcified, fibrous, lipidic and mixed plaques. Quantitative IVOCT ( qIVOCT) is necessary to provide the physiological contrast mechanisms and obtain the characteristic parameters of tissues with clinical diagnostic value. In this paper, the progress of qIVOCT is reviewed. The current methods for quantitatively measuring optical, elastic and hemodynamic parameters of vessel wall and plaque tissues using IVOCT gray-scale images and raw backscattered signals are introduced and potential development is forecast.

Cardiogenesis with a focus on vasculogenesis and angiogenesis.

The initial intraembryonic vasculogenesis occurs in the cardiogenic mesoderm. Here, a cell population of proendocardial cells detaches from the mesoderm that subsequently generates the single endocardial tube by forming vascular plexuses. In the course of embryogenesis, the endocardium retains vasculogenic, angiogenic and haematopoietic potential. The coronary blood vessels that sustain the rapidly expanding myocardium develop in the course of the formation of the cardiac loop by vasculogenesis and angiogenesis from progenitor cells of the proepicardial serosa at the venous pole of the heart as well as from the endocardium and endothelial cells of the sinus venosus. Prospective coronary endothelial cells and progenitor cells of the coronary blood vessel walls (smooth muscle cells, perivascular cells) originate from different cell populations that are in close spatial as well as regulatory connection with each other. Vasculo- and angiogenesis of the coronary blood vessels are for a large part regulated by the epicardium and epicardium-derived cells. Vasculogenic and angiogenic signalling pathways include the vascular endothelial growth factors, the angiopoietins and the fibroblast growth factors and their receptors.

Magnetic resonance imaging for pathobiological assessment and interventional treatment of the coronary arteries.

X-ray-based fluoroscopy is the standard tool for diagnostics and intervention in coronary artery disease. In recent years, computed tomography has emerged as a non-invasive alternative to coronary angiography offering detection of coronary calcification and imaging of the vessel lumen by the use of iodinated contrast agents. Even though currently available invasive or non-invasive techniques can show the degree of vessel stenosis, they are unable to provide information about biofunctional plaque properties, e.g. plaque inflammation. Furthermore, the use of radiation and the necessity of iodinated contrast agents remain unfavourable prerequisites. Magnetic resonance imaging (MRI) is a radiation-free alternative to X-ray which offers anatomical and functional imaging contrasts fostering the idea of non-invasive biofunctional assessment of the coronary vessel wall. In combination with molecular contrast agents that target-specific epitopes of the vessel wall, MRI might reveal unique plaque properties rendering it, for example, ‘vulnerable and prone to rupture’. Early detection of these lesions may allow for early or prophylactic treatment even before an adverse coronary event occurs. Besides diagnostic imaging, advances in real-time image acquisition and motion compensation now provide grounds for MRI-guided coronary interventions. In this article, we summarize our research on MRI-based molecular imaging in cardiovascular disease and feature our advances towards real-time MRI-based coronary interventions in a porcine model.

A NOVEL 3-DIMENSIONAL TECHNIQUE IN MEASURING PERICORONARY EPICARDIAL ADIPOSE TISSUE

Pericoronary epicardial adipose tissue radiodensity (PCATrd) is of emerging interest as a risk factor for coronary artery disease (CAD), but can be difficult to measure. This study aims to investigate a novel semi automated three-dimensional quantification of PCATrd. Fifty-five patients with suspected CAD were retrospectively identified. PCATrd was measured in contrast CT data-set using image analysis software (ITK-SNAP, Version 3.6.0). We applied a thresholding map, using in-house MatLab code with range of (-190,-3) Hounsfield unit derived from previous work, to the contrast CT data-set. The cursor was probed in the center of the short axis of the coronary arteries in the coronal, sagittal and axial images simultaneously. Then the 3D round brush segmented the epicardial adipose tissue with the orthogonal distance from the coronary vessel wall equal to the coronary radius and, the segmentation followed the path of 4 major coronary arteries from proximal to the distal terminal (Figure 1 A & B). The PCATrd of each coronary artery was automatically computed. We compared this 3D segmenting method (3D_PCATrd) with a 7-segment segmentation method (7S_PCATrd) published by the Society of Cardiovascular Computed Tomography. We further compared both PCATrd estimates with coronary artery disease severity (non-obstructive, obstructive and extensive obstructive) by using ordered logistic regression. The 3D_PCATrd was substantially different from the 7S_PCATrd in the general_PCATrd, LM, LAD and RCA, but similar in LCX (Table 1 & Figure 1C). Standard deviations around 3D_PCATrd estimates were significantly smaller than estimates from 7S_PCATrd. The 3D_PCATrd, but not 7S_PCATrd, was independently associated with severity of coronary lesions (multivariable odds ratio 0.86 for per 1 HU increase, p=0.017). Our novel 3-dimension quantified PCATrd technique produced estimates that were significantly different than estimates derived from the SCCT published technique, was more precise than the 7-segment quantified PCATrd and was better associated with coronary artery disease severity.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

P2798Final 5-year outcomes of the TRIAS High Risk of Restenosis; a multi-centre, randomized trial comparing endothelial progenitor cell capturing stent with drug-eluting stents

Abstract Background One of the major long-term disadvantages of percutaneous coronary intervention (PCI) remains in-stent restenosis and need for repeat revascularisation. The polymer-regulated delivery of cytotoxic or cytostatic drugs, on drug-eluting stents (DES), impede the natural healing response of the damaged vessel wall. In animals, endothelial progenitor cells (EPCs) beneficially influence the repair of the coronary vessel wall after damage by stent placement. It is hypothesized that after immobilisation the EPCs differentiate into a functional endothelial layer and that this layer will prevent neointimal proliferation and thrombus formation. Anti-CD34+ antibodies are able to capture the EPCs. The Genous stent consist of a bare-metal stent with anti-CD34+ antibody coating. Purpose Demonstrating long-term performance of Genous EPC capturing stent (ECS) relative to DES regarding target lesion failure (TLF); the composite of cardiac death, myocardial infarction (MI) and any target lesion revascularisation (TLR) within 5 years. Methods We undertook an international, clinical trial in 26 centres planning to randomise 1300 patients with stable coronary artery disease and with a high risk of restenosis between treatment with either ECS or DES. After a routine review with 50% of the patients enrolled, early cessation of the trial was recommended by the data and safety monitoring board when TLF in the ECS population was substantially higher and treatment of new patients with an ECS would be unreasonable. The trial was terminated for safety reasons. Results A total of 622 were randomly assigned to receive either Genous ECS (304 patients, 367 lesions) or DES (318 patients, 388 lesions). Five year follow-up data was obtained in 95.5% of patients. TLF occurred in 29.1% of the ECS-treated patients and in 16.0% of the DES-treated patients (p<0.001) (Figure 1). This difference was driven by higher rates of TLR (22.9% vs. 10.7%, p<0.001), but not by cardiac death (6.5% vs. 4.5%, p=0.268), or MI (5.8% vs. 3.6%, p=0.175). Definite or probable stent thrombosis was seen in 8 ECS-treated patients (2.7%) and in 3 DES-treated patients (1%), p=0.11. Figure 1. KM curves of TLF at 5year fu. Conclusion The Genous ECS is not sufficiently strong to compete with DES in terms of restenosis prevention in patients/lesions with a high risk of restenosis. If the addition of a EPCs capturing layer on a DES, like the COMBO stent, provides a lower risk of restenosis compared to DES will be tested in the ongoing SORT-OUT X trial. Acknowledgement/Funding OrbusNeich

Plaque Layer Identification in IVUS Images by Iterative based Energy Minimization of Contour Method (IEMCM)

Atherosclerotic plaque is the major cause of coronary heart artery diseases. Heart artery plaque layer analysis is one of the most important and challenging problem, which can be determined by using Intravascular Ultrasound (IVUS) Cross Sectional images, which is an excellent ultrasound study system for extracting and to easily identify the plaque layer by using the shape parameter measurements. This paper presents and elucidates the novel approach to find out the plaque layer with the help of the artery cross sectional layers determination, which are adventitia, media, intima and lumen layers. This system measures the layer’s performance to make the clear way to identify the plaque layer, which proposes a new method namely Iterative based Energy Minimization of Contour method (IEMCM). The cross sectional IVUS acts as an input image for processing and analysis of the plaque layer based on the IVUS Simulation study Measurements of coronary vessel wall dimensions and shape measurements. The proposed method produced high accuracy when compared to the existing methods.

Coronary vessel wall visualization via three-dimensional turbo spin-echo black blood imaging in Kawasaki disease

PurposeTo evaluate the feasibility of coronary vessel wall visualization using three-dimensional turbo spin-echo black blood imaging (3D-TSE) in children with Kawasaki disease. Materials and methodsNine patients (6 girls and 3 boys; mean age ± standard deviation, 5.6 ± 3.3 years; range, 1.4–10.3 years) were included. Coronary magnetic resonance angiography (MRA) with an axial slice orientation and 3D-TSE with axial and sagittal slice orientations (3D-TSE-axi and 3D-TSE-sag) were acquired for the whole heart. Coronary vessel walls were evaluated separately in aneurysm and normal-proximal regions. The internal diameter and wall thickness of the reformatted cross-sectional images were measured in both the regions. Reproducibility between MRA and 3D-TSE was evaluated via interclass correlation coefficients (ICCs) and Bland-Altman plots. ResultsIn total, 164 points (aneurysmal regions, 73; normal-proximal regions, 64; normal-distal regions, 27) were evaluated. The ICC for 3D-TSE-axi was higher than that for 3D-TSE-sag (aneurysmal regions, ICC = 0.88 and 0.81; normal-proximal regions, ICC = 0.90 and 0.32, respectively). Bland-Altman plots of the internal diameter via MRA and 3D-TSE-axi showed a wide 95% limit of agreement (−0.13 to 2.89 mm) and significant fixed and proportional biases (P < 0.001 and P = 0.002) in the aneurysmal regions. However, the 95% limit of agreement was narrow (−0.14 to 0.57 mm) in the normal-proximal regions. If 1 mm was set as the cut-off for a thickened wall, wall thickness via 3D-TSE-axi was found to be abnormal across many points (84.0% of aneurysmal regions; 18.4% of normal-proximal regions). Conclusions3D-TSE imaging of the normal-proximal regions of the coronary vessel in individuals with Kawasaki disease was found to be feasible. However, in aneurysmal regions, larger aneurysmal diameters led to an increased bias between MRA and 3D-TSE.

Sexual Dimorphism of Coronary Artery Disease in a Low- and Intermediate-Risk Asymptomatic Population: Association with Coronary Vessel Wall Thickness at MRI in Women.

To demonstrate the association between coronary vessel wall thickness (VWT) measured at MRI and coronary artery disease (CAD) risk in asymptomatic groups at low and intermediate risk on the basis of Framingham score. A total of 131 asymptomatic adults were prospectively enrolled. All participants underwent CT angiography for scoring CAD, and coronary VWT was measured at 3.0-T MRI. Nonlinear single and multivariable regression analyses with consideration for interaction with sex were performed to investigate the association of traditional atherosclerotic risk factors and VWT with CT angiography-based CAD scores. The analysis included 62 women and 62 men with low or intermediate Framingham score of less than 20%. Age (mean age, 45.0 years ± 14.5 [standard deviation]) and body mass index were not different between the groups. Age, sex, and VWT were individually significantly associated with all CT angiography-based CAD scores (P < .05). Additionally, sex was a significant effect modifier of the associations with all CAD scores. In men, age was the only statistically significant independent risk factor of CAD; in women, VWT was the only statistically significant independent surrogate associated with increased CAD scores (P < .05). In asymptomatic women, VWT MRI was the primary independent surrogate of CAD, whereas age was the strongest risk factor in men. This study suggests that VWT may be used as a CAD surrogate in women at low or intermediate risk of CAD. Further longitudinal studies are required to determine the potential implication and use of this MRI technique for the preventative management of CAD in women.© RSNA, 2019.

Coronary Vessel Wall Imaging: State of the Art and Future Directions

The purpose of this paper is to review the latest advancements and developments in non-invasive coronary magnetic resonance (MR) and hybrid positron emission tomography (PET)/MR imaging. Coronary MRI has advanced in recent years in different aspects, especially regarding technical developments, scan protocols, and molecular probes. Recently introduced hybrid PET/MR scanners have already demonstrated great potential in improving cardiovascular imaging. Coronary atherosclerosis and acute myocardial infarction remain major threats to physical health worldwide. Several techniques, from invasive intravascular imaging to non-invasive imaging methods, are studied extensively to identify patients with vulnerable plaques at risk for adverse coronary events. While imaging of vulnerable plaques is getting more and more sophisticated, the clinical impact of molecular plaque imaging on prognosis and disease management still has to be fully defined.

Eosinophilic inflammation in spontaneous coronary artery dissection: A potential therapeutic target?

Spontaneous coronary artery dissection (SCAD), defined as non-traumatic, non-iatrogenic dissociation of coronary vessel wall resulting from intimal disruption or intramural hemorrhage, represents an important cause of sudden death and myocardial infarction among young or middle-aged women without conventional risk factors for atherosclerosis. On histopathological examination, SCAD is featured by prominent eosinophilic infiltration of the adventitia or periadventitial layer of coronary artery. It has been estimated that approximately 15–30% of SCAD patients experience recurrent episodes of dissection despite medical therapy. Preliminary evidence suggests that injury to the vascular endothelium and myocytes in the arterial wall may be explained by cytotoxic products released from eosinophils in response to inflammatory mediators. In addition, neovascularization of vasa vasorum and dilatation of intimal capillaries may be stimulated by localized eosinophils. Newly formed fragile vasa vasorum may disrupt due to high intraluminal pressure from the interconnected capillary network, leading to the expansion of intramural hemorrhage. It is hypothesized that anti-inflammatory therapy targeting eosinophilic coronary periarteritis would be effective in preventing the recurrence of SCAD by promoting the healing of dissection. The article delineates the biological plausibility, empirical data, and future perspective regarding eosinophilic inflammation as a potential therapeutic target for SCAD.

A Survey on Coronary Atherosclerotic Plaque Tissue Characterization in Intravascular Optical Coherence Tomography.

Atherosclerotic plaque deposition within the coronary vessel wall leads to arterial stenosis and severe catastrophic events over time. Identification of these atherosclerotic plaque components is essential to pre-estimate the risk of cardiovascular disease (CVD) and stratify them as a high or low risk. The characterization and quantification of coronary plaque components are not only vital but also a challenging task which can be possible using high-resolution imaging techniques. Atherosclerotic plaque components such as thin cap fibroatheroma (TCFA), fibrous cap, macrophage infiltration, large necrotic core, and thrombus are the microstructural plaque components that can be detected with only high-resolution imaging modalities such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT). Light-based OCT provides better visualization of plaque tissue layers of coronary vessel walls as compared to IVUS. Three dominant paradigms have been identified to characterize atherosclerotic plaque components based on optical attenuation coefficients, machine learning algorithms, and deep learning techniques. This review (condensation of 126 papers after downloading 150 articles) presents a detailed comparison among various methodologies utilized for plaque tissue characterization, classification, and arterial measurements in OCT. Furthermore, this review presents the different ways to predict and stratify the risk associated with the CVD based on plaque characterization and measurements in OCT. Moreover, this review discovers three different paradigms for plaque characterization and their pros and cons. Among all of the techniques, a combination of machine learning and deep learning techniques is a best possible solution that provides improved OCT-based risk stratification.

Assessment of superficial coronary vessel wall deformation and stress: validation of in silico models and human coronary arteries in vivo.

Cyclic biomechanical stress at the lumen-intima interface plays a crucial role in the rupture of coronary plaque. We performed a comprehensive assessment of a novel angiography-based method for four-dimensional (4D) dynamic assessment of superficial wall stress (SWS) and deformation with a total of 32 analyses in virtual stenosis models with equal lumen dimensions and 16 analyses in human coronary arteries in vivo. The in silico model analyses demonstrated that the SWS, derived by the proposed global displacement method without knowledge of plaque components or blood pressure, was comparable with the result calculated by traditional finite element method. Cardiac contraction-induced vessel deformation increased SWS. Softer plaque and positive arterial remodeling, associated with a greater plaque burden, showed more variation in mean lumen diameter within the cardiac cycle and resulted in higher SWS. In vivo patient analyses confirmed the accuracy of computed superficial wall deformation. The centerlines predicted by our method at random selected time instant matched well with the actual one in angiograms by Procrustes analysis (scaling: 0.995 ± 0.018; dissimilarity: 0.007 ± 0.014). Over 50% of the maximum SWS occurred at proximal plaque shoulders. This novel 4D approach could be successfully to predict superficial wall deformation of coronary artery in vivo. The dynamic SWS might be more realistic to evaluate the risk of plaque rupture.

In vivo serial invasive imaging of the second-generation drug-eluting absorbable metal scaffold (Magmaris — DREAMS 2G) in de novo coronary lesions: Insights from the BIOSOLVE-II First-In-Man Trial

RationaleBioresorbable scaffolds may confer clinical benefit in long-term studies; early mechanistic studies using intravascular imaging have provided insightful information about the immediate and mid-term local serial effects of BRS on the coronary vessel wall. ObjectivesWe assessed baseline, 6- and 12-month imaging data of the drug-eluting absorbable metal scaffold (DREAMS 2G). Methods and resultsThe international, first-in-man BIOSOLVE-II trial enrolled 123 patients with up to 2 de novo lesions (in vessels of 2.2 to 3.7mm). Angiographic based vasomotion, curvature and angulation were assessed; intravascular ultrasound (IVUS) derived radiofrequency (RF) data analysis and echogenicity were evaluated; optical coherence tomography (OCT) attenuation and backscattering analysis were also performed.There was hardly any difference in curvature between pre-procedure and 12months (−0.0019; p=0.48). The change in angulation from pre- to 12months was negligible (−3.58°; 95% CI [−5.97, −1.20]), but statistically significant. At 6months, the change in QCA based minimum lumen diameter in response to high dose of acetylcholine and IVUS-RF necrotic core percentage showed an inverse relationship (estimate of −0.489; p=0.055) and with fibrous volume a positive relationship (estimate of 0.53, p=0.035). Bioresorption analysis by OCT showed that the maximum attenuation values decreased significantly from post-procedure at 6months (Δ 6months vs. post-proc. is −13.5 [95% CI −14.6, −12.4]) and at 12months (Δ 12months vs. post-proc. is −14.0 [95% CI −15.4, −12.6]). By radiofrequency data, the percentage of dense calcium decreased significantly from post-procedure at 6months and at 12months. Likewise, by echogenicity, hyperechogenic structures decreased significantly from post-procedure at 6months; thereafter, they remained unchanged. ConclusionFollowing implantation of DREAMS 2G, restoration of the vessel geometry, vasomotion and bioresorption signs were observed at up to 12months; importantly, these changes occurred with preservation of the lumen size between 6 and 12months.NCT01960504

Contrast-enhanced magnetic resonance imaging for the detection of ruptured coronary plaques in patients with acute myocardial infarction.

PurposeX-ray coronary angiography (XCA) is the current gold standard for the assessment of lumen encroaching coronary stenosis but XCA does not allow for early detection of rupture-prone vulnerable plaques, which are thought to be the precursor lesions of most acute myocardial infarctions (AMI) and sudden death. The aim of this study was to investigate the potential of delayed contrast-enhanced magnetic resonance coronary vessel wall imaging (CE-MRCVI) for the detection of culprit lesions in the coronary arteries.Methods16 patients (13 male, age 61.9±8.6 years) presenting with sub-acute MI underwent CE-MRCVI within 24-72h prior to invasive XCA. CE-MRCVI was performed using a T1-weighted 3D gradient echo inversion recovery sequence (3D IR TFE) 40±4 minutes following the administration of 0.2 mmol/kg gadolinium-diethylenetriamine-pentaacetic acid (DTPA) on a 3T MRI scanner equipped with a 32-channel cardiac coil.Results14 patients were found to have culprit lesions (7x LAD, 1xLCX, 6xRCA) as identified by XCA. Quantitative CE-MRCVI correctly identified the culprit lesion location with a sensitivity of 79% and excluded culprit lesion formation with a specificity of 99%. The contrast to noise ratio (CNR) of culprit lesions (9.7±4.1) significantly exceeded CNR values of segments without culprit lesions (2.9±1.9, p<0.001).ConclusionCE-MRCVI allows the selective visualization of culprit lesions in patients immediately after myocardial infarction (MI). The pronounced contrast uptake in ruptured plaques may represent a surrogate biomarker of plaque activity and/or vulnerability.

Accelerated 3D Coronary Vessel Wall MR Imaging Based on Compressed Sensing with a Block-Weighted Total Variation Regularization

Coronary vessel wall magnetic resonance (MR) imaging is important for heart disease diagnosis but often suffers long scan time. Compressed sensing (CS) has been previously used to accelerate MR imaging by reconstructing an MR image from undersampled k-space data using a regularization framework. However, the widely used regularizations in the current CS methods often lead to smoothing effects and thus are unable to reconstruct the coronary vessel walls with sufficient resolution. To address this issue, a novel block-weighted total variation regularization is presented to accelerate the coronary vessel wall MR imaging. The proposed regularization divides the image into two parts: a region-of-interest (ROI) which contains the coronary vessel wall, and the other region with less concerned features. Different penalty weights are given to the two regions. As a result, the small details within ROI do not suffer from over-smoothing while the noise outside the ROI can be significantly suppressed. Results with both numerical simulations and in vivo experiments demonstrated that the proposed method can reconstruct the coronary vessel wall from undersampled k-space data with higher qualities than the conventional CS with the total variation or the edge-preserved total variation.

Effects of moderate‑intensity endurance exercise on angiotensin II and angiotensin II type I receptors in the rat heart.

The current study was aimed at examining the effects of moderate-intensity endurance exercise on the expression of angiotensin II (AngII) and AngII type 1 receptor (AT1R) in the rat heart. Male Sprague-Dawley rats were randomly divided into the control group (n=20) and moderate-intensity endurance exercise group (n=20). Cardiac hypertrophy was induced by treadmill endurance training for 8 weeks. The mRNA expression of AngII and AT1R were assessed by reverse transcription-quantitative polymerase chain reaction. The immune response positive area and optical density of AngII and AT1R was measured by immunohistochemistry. AngII was primarily expressed in the cytoplasm and membrane, however infrequently in coronary vascular wall smooth muscle cells. AT1R was primarily expressed in the coronary vessel wall smooth muscle, rarely in cardiac cells. The mRNA expression of cardiac AngII was significantly increased after the 8-week exercise period, while AT1R was significantly decreased. Immunohistochemistry indicated a significant increase in the AngII immune-positive area and optical density after the 8-week exercise. The AT1R immune-positive area and optical density was significantly reduced following the 8-week exercise. In conclusion, subsequent to 8-weeks endurance training, the AngII expression was increased and the AT1R expression was decreased. AT1R may expand the coronary artery, thereby increasing coronary blood flow and ensuring the energy supply of heart during exercise. The expression change in AngII does not reflect the character of cardiac hypertrophy. The exercise-induced change in the expression of AngII and AT1R may be a protective mechanism to avoid cardiac pathological hypertrophy.

Superficial wall stress assessed from 4-D analysis of coronary angiography in vivo

Acute coronary events are frequently caused by plaque rupture or plaque erosion. The mechanisms involved imply mechanical forces that act upon superficial plaque layers. Analyses of the stress to the superficial coronary vessel wall may help understand the mechanisms involved and might ultimately allow assessing pharmacological approaches aimed at increasing the biomechanical stability of plaques. We recently developed a novel approach of 4-dimensional (4D) analysis of superficial wall stress (SWS) on coronary arteries by combining imaging processing with a semi-inverse finite element method (Fig. 1). Angiographic reconstruction was performed to reconstruct the interrogated vessel at several phases of the cardiac cycle. Then, the motion trajectory of each node during heartbeat is implemented by its respective displacement loads, determined by optimal node-to-node mapping between adjacent finite element configurations. This approach does not need to delineate plaque components and structures or to implement data on dynamic blood pressure, as the complex interaction thereof is intrinsically incorporated in the cyclic changes in lumen geometries, which are used as inputs to compute SWS by the proposed approach. Pending validation, this novel approach may be used as a tool to evaluate superficial coronary wall stress and its potential impact on future coronary events.