Assessment of vasa vasorum on coronary plaques in patients with acute coronary syndromes using intravascular ultrasound and iMap analysis: A retrospective cohort study.

Studies have revealed that vasa vasorum (VV) neovascularization is vital for the progression and vulnerability of coronary atherosclerotic plaques. The correlation between VV, plaque constituents, and the no-reflow phenomenon (NRP) in percutaneous coronary intervention (PCI) remains elusive. We explored plaque constituents in iMap-intravascular ultrasound (iMap-IVUS) and NRP during PCI for VV lesions. We studied 166 coronary lesions in 166 patients with acute coronary syndromes (ACS) (118 lesions with VV) undergoing pre-intervention intravascular ultrasound (IVUS). We evaluated the diversity in plaque morphological status and post-PCI results based on the presence or absence of VV. The lesions with VV group had significantly higher high-sensitivity C-reactive protein (hs-CRP) levels than the lesions without VV group (8.41 ± 4.98 vs 4.19 ± 3.69 mg/L, P < .001). The frequency of after-stent deployment thrombolysis in myocardial infarction (TIMI) flow grades 0, 1, and 2 was remarkably greater in lesions with VV than in those without VV (22.9% vs 10.4%, P < .001). Plaques at the minimum lumen, necrotic core (1.26 ± 0.64 vs 0.92 ± 0.61 mm2, P < .001; 20.95 ± 7.19 vs 13.34% ± 6.54%, P < .001), and fibrous areas (4.23 ± 1.32 vs 3.92 ± 1.01 mm2, P = .006; 61.01 ± 9.41 vs 56.92% ± 11.42%, P = .001) were considerably larger in the lesions with VV than in those without VV. In addition, densely calcified plaques (0.41 ± 0.26 vs 0.81 ± 0.59 mm2, P < .001; 3.63 ± 2.19 vs 7.18% ± 2.01%, P < .001) were considerably smaller in the lesions with VV than in those without VV. Multivariate analyses revealed that VV and plaque volume were independent predictors of NRP after stent deployment (odds ratio [OR]: 5.13, 95% confidence interval [CI]: 1.19-15.32, P = .002; OR: 4.79, 95% CI: 1.08-9.01, P = .005). Lesions with VV exhibited considerable plaque vulnerability in patients with ACS, and they displayed more NRP during PCI. VV and plaque volume were independent predictors of NRP after stent deployment.

Non-invasive imaging techniques and assessment of carotid vasa vasorum neovascularization: Promises and pitfalls.

Carotid adventitia vasa vasorum neovascularization (VVn) is associated with the initial stages of arteriosclerosis and with the formation of unstable plaque. However, techniques to accurately quantify that neovascularization in a standard, fast, non-invasive, and efficient way are still lacking. The development of such techniques holds the promise of enabling wide, inexpensive, and safe screening programs that could stratify patients and help in personalized preventive cardiovascular medicine. In this paper, we review the recent scientific literature pertaining to imaging techniques that could set the stage for the development of standard methods for quantitative assessment of atherosclerotic plaque and carotid VVn. We present and discuss the alternative imaging techniques being used in clinical practice and we review the computational developments that are contributing to speed up image analysis and interpretation. We conclude that one of the greatest upcoming challenges will be the use of machine learning techniques to develop automated methods that assist in the interpretation of images to stratify patients according to their risk.

In vivo assessment of vasa vasorum neovascularization using intravascular ultrasound: A comparison between acute coronary syndrome and stable angina pectoris.

BACKGROUND: Previous studies have suggested that vasa vasorum (VV) neovascularization plays an important role in the progression and vulnerability of coronary atherosclerotic plaque. METHODS: A total of 130 patients with coronary artery disease including 75 acute coronary syndrome (ACS) cases and 55 stable angina pectoris (SAP) cases were studied. By using intravascular ultrasound (IVUS), VV was defined as a small (<1mm) tubular or vesicular, low-echoic structure observed exterior to the media. Prevalence and maximal number of VV were compared between patients with ACS versus SAP. RESULTS: The prevalence of VV at the culprit lesion was similar between the 2 groups (97% vs. 93%, p=0.216). On the other hand, it was significantly higher in ACS than SAP at both reference sites (proximal: 93% vs. 81%, p=0.047 and distal: 88% vs. 60%, p<0.001, respectively). The maximum number of VV was significantly higher in ACS than in SAP (at the culprit lesion: 2.8±1.3 vs. 1.8±1.0, p<0.001, at the proximal reference: 1.9±1.1 vs. 1.3±0.9, p=0.003 and distal reference: 1.7±1.1 vs. 1.1±1.1, p=0.003, respectively). CONCLUSIONS: VV neovascularization of coronary arteries was more enhanced in patients with ACS than in those with SAP, supporting its relation to plaque vulnerability. VV detected by widely used IVUS could be an adequate surrogate marker for plaque vulnerability in vivo.

Assessment of vasa vasorum in the walls of thrombophlebitic saphenous vein.

AIM: The purpose of this study was to investigate the proliferation of vasa vasorum (VV) in the walls of thrombophlebitic saphenous vein (TSV), and to evaluate the influence of high venous pressure and lack of oxygen on the VV. METHODS: The specimens of the great saphenous vein were collected: 11 primary varicose vein (PVV), 11 TSV and, as a control, eight normal great saphenous vein. Masson staining and immunohistochemistry for CD34 were used to observe the status of VV, and the number of VV were counted under light microscopy. RESULTS: VV of the thrombophlebitic saphenous vein group (TSVG) were clustered together in adventitia, increased linearly in media, and scattered appearance in intima, were increased partially in intima of thrombus rupturing. In TSVG, the number of VV observed in adventitia, media and intima was 16.738±7.685, 4.845±2.537, 2.448±3.030, respectively. In the primary varicose vein group (PVVG), the corresponding values were 14.280±4.440, 2.965±1.125, 0.500±0.548. And the number was 8.911±2.629, 0.150±0.424, 0±0 in the control group (CG). Significantly higher numbers of VV were observed in the TSVG as compared to the PVVG or CG (P<0.05). No significant difference was observed between intima and media (P>0.05). CONCLUSION: Thrombi in varicose veins can induce proliferation of VV, which may be involved in high venous pressure and hypoxia.

Analysis of contrast-enhanced intravascular ultrasound images for the assessment of coronary plaque neoangiogenesis: another step closer to the identification of the vulnerable plaque.

Atherosclerotic cardiovascular disease (CVD), primarily manifested as heart attacks and strokes, remains the main cause of death in the developed countries and is rapidly increasing in the developing world. Early detection and aggressive treatment of hidden (asymptomatic) atherosclerotic plaques that cause heart attack or stroke are most needed. However, existing clinical tools are not sufficient to address this need. Intravascular ultrasound (IVUS) is a catheter-based medical imaging tool that is capable of providing cross-sectional images of arteries. It is by far the most powerful clinical tool available for characterization of atherosclerotic plaques. However, existing IVUS is unable to detect plaque inflammation which is a key factor in complications of atherosclerotic plaques. Contrast enhanced IVUS (CE-IVUS) for detection of Vasa Vasorum (VV), microvessles that feed the vessel wall, can indirectly image plaque inflammation and thereby significantly increase the diagnostic power of IVUS. Several studies have shown that the density of VV in the atherosclerotic plaques is strongly correlated with the intensity of plaque inflammation and related processes which lead to plaque destabilization and rupture (the Vulnerable Plaque). Therefore the detection and measurement of VV in plaque, and leakage of blood from VV into plaques using CE-IVUS, can enable the development of an index for plaque vulnerability. In this paper, we present a review of our original work on coronary VV imaging, discuss subsequent reports by others, and also present the latest on the detection of VV based on CE-IVUS.

A new method for assessment of plaque vulnerability based on vasa vasorum imaging, by using contrast-enhanced intravascular ultrasound and differential image analysis.

BACKGROUND: Increased neovascularization in vasa vasorum and atherosclerotic plaques has recently been identified as a common feature of inflammation and plaque vulnerability. Microbubble contrast agents, which have been used for intravascular imaging, can be used to trace neovascularization. The aim of the study was to detect and evaluate the density of vasa vasorum in non-culprit coronary atherosclerotic plaques of patients with acute coronary syndrome. METHODS: We have studied intravascular ultrasound (IVUS) signals before, during, and after intracoronary injection of microbubbles, proximal to non-culprit atherosclerotic plaques in 16 patients with acute coronary syndrome. Analyses were accomplished using a computational algorithm for the detection of contrast perfusion in such contrast-enhanced sequences. Perfusion density was evaluated by the mean enhancement in the region of interest provided by this difference-imaging technique. RESULTS: Qualitative and quantitative analysis of the pre- and post-injection images showed a significant enhancement in the grey-scale intensity of intima-media and adventitia after injection (intima-media: from 6.0+/-2.5 to 7.9+/-3.3%, p=0.006 and adventitia: from 7.1+/-2.2 to 7.6+/-2.5%, p=0.035). CONCLUSIONS: Contrast-enhanced intravascular imaging is a novel, yet clinically available, technique that has the potential to enhance IVUS-based characterization of atherosclerotic plaques. The technique introduces a new perspective to the detection of vulnerable plaques and warrants further investigations.

Contrast-enhanced intravascular ultrasound: combining morphology with activity-based assessment of plaque vulnerability.

Acute coronary syndromes are the result of coronary plaque rupture in the majority of cases. Available diagnostic techniques that focus on the early detection of plaques that are prone to rupture are still limited. Increased neovascularization in the vasa vasorum of the atherosclerotic plaque has been identified recently as a common feature of inflammation and plaque vulnerability. Microbubbles, which have been used for ultrasound imaging, can be used to trace neovascularization. We present recent advances in contrast agents and contrast-enhanced intravascular ultrasound that may be used for the detection of vasa vasorum, including fundamental and harmonic contrast imaging. Identification of vasa vasorum proliferation in atherosclerotic plaques presents important clinical implications; in particular it could provide a means to detect vulnerability in vivo, thereby guiding targeted treatments.