This study investigates methodological variability across various expert laboratories worldwide, with regards to characterizing the mechanical properties of biological tissues. Two testing rounds were conducted on the specific use case of uniaxial tensile testing of porcine aorta. In the first round, 24 labs were invited to apply their established methods to assess inter-laboratory variability. This revealed significant methodological diversity and associated variability in the stress–stretch results, underscoring the necessity for a standardized approach. In the second round, a consensus protocol was collaboratively developed and adopted by 19 labs in an attempt to minimize variability. This involved standardized sample preparation and uniformity in testing protocol, including the use of a common cutting and thickness measurement tool. Despite protocol harmonization, significant variability persisted across labs, which could not be solely attributed to inherent biological differences in tissue samples. These results illustrate the challenges in unifying testing methods across different research settings, underlining the necessity for further refinement of testing practices. Enhancing consistency in biomechanical experiments is pivotal when comparing results across studies, as well as when using the resulting material properties for in silico simulations in medical research.

Atherosclerosis is a chronic inflammatory and metabolic disease primarily driven by systemic lipid imbalances, with plaque localization and progression further modulated by local hemodynamic and cellular factors within the arterial wall. Here we present a validation study of a hybrid multiscale model that couples computational fluid dynamics (CFD), mass-transport-driven low-density lipoprotein (LDL) maps, and an agent-based model (ABM) of cell behavior to predict coronary plaque initiation and progression. Validation employed adult minipigs carrying a low-density lipoprotein receptor (LDLR) mutation—an established preclinical analogue of human hypercholesterolemia—using longitudinal in vivo imaging data collected within the BIOCCORA study, with 1-year follow-up capturing plaque initiation and evolution. By linking wall shear stress (WSS)-dependent LDL filtration with cytokine-guided smooth muscle cell (SMC) activity, the model mechanistically reconstructs the plaque microenvironment rather than fitting outcomes post hoc. Tested on four imaging-derived porcine coronary arteries tracked over time, the model anticipates where and how fast plaques grow and how lipid pools evolve across cross-sections, showing strong concordance with experiments. These results position hybrid multiscale in silico models as promising predictors for disease progression and could aid in future treatment decision-making.

Rationale and Objectives: While calcification is a highly prevalent component in atherosclerotic extracranial carotid arteries and is known to impact plaque stability, the link between carotid calcification and ischemic events is yet to be identified. We aimed to investigate the associations of geometric features of carotid calcifications, and their temporal changes, with ischemic events. Materials and Methods: We retrospectively analyzed 128 mildly stenotic carotid arteries (Plaque At Risk study) from 64 patients with recent ischemic event, using multi-detector computed tomography angiography data at baseline and after 2 years. The 3D artery and calcification geometries were reconstructed with a semi-automatic pipeline, and an in-depth calcification morphometric assessment was performed. We examined the distribution of the calcification morphometrics and their temporal changes and investigated their associations with ischemic events at the time of inclusion, using generalized linear mixed models. Results: At baseline, compared to contralateral asymptomatic arteries, symptomatic carotids had more calcification bodies (mean [95%CI]: 1.9 [1.4–2.6] vs. 1.6 [1.2–2.2]). These calcifications were smaller (mean area [95%CI]: 3.7 mm² [2.9–5.1] vs. 4.5 mm² [3.5–5.8]) and narrower (mean width [95%CI]: 2.7 mm [2.3–3.4] vs. 3.1 mm [2.5–3.6]). At 2-year follow-up, adjusting for baseline measurements, these calcifications were smaller (mean width [95%CI]: 2.9 mm [2.5–3.5] vs. 3.3 mm [2.7–3.7]) and longer (mean [95%CI]: 8.6 mm [7.1–10.5] vs. 7.5 mm [6.3–9.5]) compared to asymptomatic side. Conclusion: Symptomatic carotid arteries presented more and smaller calcifications with a tendency to grow more in the longitudinal artery direction, providing insights into the role of carotid calcifications in ischemic events.

Rupture of the cap of an atherosclerotic plaque can trigger thrombotic cardiovascular events. It has been suggested, through computational models, that the presence and specific location of microcalcifications in the atherosclerotic cap can increase the risk of cap rupture. However, the experimental confirmation of this hypothesis is lacking. In this study, we investigated how the presence and location of microcalcifications, relative to the lumen, influence (local) mechanics and rupture behavior of atherosclerotic plaque caps. Using tissue-engineered fibrous cap analogs with hydroxyapatite (HA) clusters to mimic calcifications in human plaque caps, we replicated the microcalcification distribution observed in human carotid plaques, as identified by our histological analysis. The analogs were imaged using multiphoton microscopy with second-harmonic generation to assess local collagen fiber orientation and dispersion. Subsequently, they underwent uniaxial tensile testing to failure, during which local strain and failure characteristics were analyzed. Our results revealed that HA clusters, particularly those in the luminal region, contribute to increased local collagen fiber dispersion. Moreover, the presence of HA clusters reduced both failure tensile stress and strain in the TE cap analogs. Besides, the rupture location shifted toward the site of HA clusters. Additionally, rupture initiation was consistently found in high-strain regions, and in 86 % of the analogs, even at the highest strain location in the sample. Our findings suggest that microcalcification clusters in plaque caps may increase the cap rupture risk and relocate the rupture site. Moreover, local strain measurements can serve as an additional tool for plaque cap rupture risk assessment.

Background and aims: Local biomechanical factors are known to influence atherosclerosis in extracranial carotid arteries. While the role of some flow-driven biomechanical factors has been investigated, the influence of pressure-driven mechanical wall stress (MWS) has received limited attention. In this study, the association of the pressure-driven and flow-driven biomechanical factors with carotid atherosclerosis was examined. Methods: Carotid arteries (n = 150) with mild-to-moderate stenosis from 75 symptomatic patients (Plaque-At-Risk study) were imaged using multi-detector computed tomography angiography (MDCTA) at the time of inclusion and after 2 years. Structural changes in carotid wall and calcifications were quantified from MDCTA data while the local baseline biomechanical factors in the carotids were determined using fluid-structure interaction (FSI) computational models. The associations of the local pressure-driven and flow-driven biomechanical factors with the carotid wall and calcification changes were studied using Generalized Linear Mixed models. Results: Over two years, plaque sectors, with calcified and non-calcified sectors combined, exhibited minimal change in wall thickness, likely due to medical treatment. High MWS was associated (p < 0.001) with a reduction in plaque thickness. In calcified plaque sectors, high MWS and low oscillatory shear index (OSI) were associated (p < 0.001) with greater calcification thickness increase. The distance between the lumen and calcification decreased over time, especially in the sectors exposed to high time-averaged wall shear stress (TAWSS) and high MWS. Conclusions: Our results suggest that the pressure-driven local MWS and flow-driven OSI and TAWSS significantly correlate with the development of calcified and non-calcified plaques in carotid arteries. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01208025.

Background and objective: Although the association of wall shear stress (WSS) with coronary artery disease has been well studied, that of mechanical wall stress (MWS) is mainly overlooked. In this study, we performed in-silico artery-specific modeling to investigate the involvement of both MWS and WSS in coronary artery disease. Methods: Fifteen coronary arteries from five adult familial hypercholesterolemic pigs were imaged by coronary computed tomography angiography, intravascular ultrasound, and optical coherence tomography at three time points (3, 9, and 12 months). Local WSS and MWS in 3 mm/45° sectors were determined using artery-specific computational models. The relationship of WSS and MWS with wall thickness change (ΔWT) over time was statistically analyzed using Generalized Linear Mixed models. Results: A positive ΔWT was measured in all sectors, where plaque sectors presented a greater ΔWT rate compared to plaque-free sectors. In plaque-free sectors, low WSS was associated with a higher ΔWT rate (p < 0.001). In plaque sectors, high MWS was associated with a higher ΔWT rate (p < 0.05), where ΔWT rate was, although slightly, even greater in the plaque sectors with lipid-rich necrotic core (p < 0.05). Conclusions: Our results from in-silico coronary-specific models suggest that WSS and MWS may play a dominant role at different stages of coronary artery disease. WSS may be more critical in the early stages of plaque formation while MWS might have greater significance in the progression of existing plaques.

Background: Intracranial artery calcification detected on CT imaging is a recognized risk factor for ischemic cerebrovascular diseases, but the underlying etiology of this association remains unclear. Differences in objective morphometric characteristics of these calcifications may partially explain this association, yet these measurements are largely absent in the literature. We investigated intracranial artery calcification morphometry in patients with recent anterior ischemic stroke or TIA, assessing potential differences between calcifications in both intracranial carotid arteries (ICAs) located ipsilateral and contralateral to the cerebral ischemia. Methods: Among 100 patients (mean age 69.6 (SD 8.8) years) presenting to academic neurology departments, 3D reconstructions of both ICAs were based on clinical CT-angiography images. On these reconstructions, a luminal centerline and cross-sections perpendicular to this centerline were created, facilitating the assessment of calcification morphometry, spatial orientation and stenosis severity. Differences in calcification characteristics between ICAs were assessed using two-sided Wilcoxon signed-rank and χ² tests. Results: Among 200 arteries, a median of four (IQR 2–6) individual calcifications were counted, with a mean area of 1.8 (IQR 1.2–2.7) mm², a mean arc width of 43.5 (IQR 32.3–53.2) degrees, and median longitudinal extent of 15.4 (IQR 5.9–27.0) mm. Calcifications were most often present in the anatomical C4 section (56.0%), with predominantly posterosuperior orientation (38.5%) and 42.0% had a local stenosis severity > 70%. None of these aspects significantly differed between ICAs, and this remained after restricting analyses to patients with undetermined etiology. Conclusions: We found no differences in morphometrical or spatial aspects of calcifications between ICAs ipsilateral and contralateral to the cerebral ischemia.

In-stent restenosis represents a major cause of failure of percutaneous coronary intervention with drug-eluting stent implantation. Computational multiscale models have recently emerged as powerful tools for investigating the mechanobiological mechanisms underlying vascular adaptation processes during in-stent restenosis. However, to date, the interplay between intervention-induced inflammation, drug delivery and drug retention has been under-investigated. Here, an original patient-specific multiscale agent-based modelling framework was developed to investigate the interplay between drug release, plaque composition and intervention-induced inflammation on in-stent restenosis following drug-eluting stent implantation. The framework integrated a finite element simulation of stent expansion, with a drug transport simulation and an agent-based model of cellular dynamics. A patient-specific coronary cross-section with heterogeneous diseased tissue was considered and rigorously analyzed through a variety of scenarios, including different plaque compositions and different inflammatory responses. The analysis revealed three significant findings: (i) calcifications substantially impeded drug transport, resulting in drug-depleted regions and reduced stent efficacy; (ii) by impacting drug transport, variations in plaque composition influenced arterial wall response, with the fully-calcific scenario showing the greatest lumen area reduction; (iii) the impact of different drug receptor saturation conditions (obtained with different plaque compositions) was particularly evident under conditions of persistent inflammatory state. This study represents a significant advancement in multiscale modelling of in-stent restenosis following drug-eluting stent implantation. The results obtained provided deeper insights into the complex interactions among patient-specific plaque composition, inflammation and drug retention, suggesting a patient-specific management of the intervention, particularly in cases of complex disease.

Introduction: Ischemic stroke incidence varies significantly with respect to sex and cardiovascular risk factors (CVRFs), a relationship that it is not well understood. Calcification in carotid atherosclerosis is known to impact plaque stability, potentially linked to ischemic stroke. The objective was to assess the in-depth calcification morphometrics within extracranial carotid atherosclerosis, their temporal changes, and associations with sex and CVRFs. Methods: Carotid arteries (n = 144) with confirmed atherosclerosis and mild-to-moderate stenosis from 72 symptomatic patients (Plaque-At-Risk study) with recent ischemic event due to ischemia in the territory of a carotid artery were imaged using multidetector computed tomography angiography (MDCTA) at baseline and after 2 years. The lumen, vessel wall, and calcifications were segmented semiautomatically, and the carotid geometries were 3D reconstructed. A comprehensive morphometric assessment of carotid calcifications was performed on the baseline and followup scans. We investigated distributions of these metrics and their associations with sex and CVRFs using generalized linear mixed models. Results: Our findings suggest that women have larger (4.5 mm2 [95% CI: 3.2-6.2] vs. 3.2 mm2 [95% CI: 2.4-4.2]) calcifications, located closer to the lumen (0.6 mm [95% CI: 0.4-0.8] vs. 0.9 mm [95% CI: 0.7-1.2]) in contrast to men at baseline and follow-up, adjusted for baseline measurements. At the baseline, nonsmokers had larger (5.3 mm2 [95% CI: 3.7-7.5] vs. 3.2 mm2 [95% CI: 2.3-4.4]) and longer (5.7 mm [95% CI: 4.1-7.3] vs. 2.4 mm [95% CI: 1.6-3.6]) calcifications than the current smokers. Diabetic patients had thicker (1.1 mm [95% CI: 0.8-1.3] vs. 0.8 mm [95% CI: 0.7-0.9]) carotid calcifications at baseline. Conclusion: Our in-depth analyses exposed several geometric features of carotid calcifications associated with sex and CVRFs and provided further insight into the pathophysiology of carotid atherosclerosis.

Many cardiovascular events are triggered by fibrous cap rupture of an atherosclerotic plaque in arteries. However, cap rupture, including the impact of the cap's structural components, is poorly understood. To obtain better mechanistic insights in a biologically and mechanically controlled environment, we previously developed a tissue-engineered fibrous cap model. In the current study, we characterized the (local) structural and mechanical properties of these tissue-engineered cap analogs. Twenty-four collagenous cap analogs were cultured. The analogs were imaged with multiphoton microscopy with second-harmonic generation to obtain local collagen fiber orientation and dispersion. Then, the analogs were mechanically tested under uniaxial tensile loading until failure, and the local deformation (strain) and failure characteristics were analyzed. Our results demonstrated that the tissue-engineered analogs mimic the dominant (circumferential) fiber direction of human plaques. The analogs also exhibited a physiological strain stiffening response, similar to human fibrous plaque caps. Ruptures in the analogs initiated in and propagated towards local high-strain regions. The local strain values at the rupture sites were similar to the ones reported for carotid human fibrous plaque tissue. Finally, the study revealed that the rupture propagation path in the analogs followed the local fiber direction. Statement of significance: Many cardiovascular events are triggered by mechanical rupture of atherosclerotic plaque caps. Yet, cap rupture mechanics is poorly understood. This is mainly due to the scarcity of plaques for high-throughput testing and the structural complexity of plaques. To overcome this, we previously developed tissue-engineered cap analogs. The current study characterizes (local) structural and mechanical properties of these cap analogs. Our findings show that: (1) cap analogs closely mimic human fibrous caps, including fiber orientation and strain stiffening responses; (2) structural and mechanical properties of cap analogs are associated, which provides critical information for understanding plaque rupture; and (3) cap ruptures commonly start in and propagate towards high-strain areas, indicating the potential use of strain measurements for cap rupture risk assessment.

The rupture of an atherosclerotic plaque cap overlying a lipid pool and/or necrotic core can lead to thrombotic cardiovascular events. In essence, the rupture of the plaque cap is a mechanical event, which occurs when the local stress exceeds the local tissue strength. However, due to inter- and intra-cap heterogeneity, the resulting ultimate cap strength varies, causing proper assessment of the plaque at risk of rupture to be lacking. Important players involved in tissue strength include the load-bearing collagenous matrix, macrophages, as major promoters of extracellular matrix degradation, and microcalcifications, deposits that can exacerbate local stress, increasing tissue propensity for rupture. This review summarizes the role of these components individually in tissue mechanics, along with the interplay between them. We argue that to be able to improve risk assessment, a better understanding of the effect of these individual components, as well as their reciprocal relationships on cap mechanics, is required. Finally, we discuss potential future steps, including a holistic multidisciplinary approach, multifactorial 3D in vitro model systems, and advancements in imaging techniques. The obtained knowledge will ultimately serve as input to help diagnose, prevent, and treat atherosclerotic cap rupture.

Endovascular thrombectomy procedures are significantly influenced by the mechanical response of thrombi to the multi-axial loading imposed during retrieval. Compression tests are commonly used to determine compressive ex vivo thrombus and clot analogue stiffness. However, there is a shortage of data in tension. This study compares the tensile and compressive response of clot analogues made from the blood of healthy human donors in a range of compositions. Citrated whole blood was collected from six healthy human donors. Contracted and non-contracted fibrin clots, whole blood clots and clots reconstructed with a range of red blood cell (RBC) volumetric concentrations (5–80%) were prepared under static conditions. Both uniaxial tension and unconfined compression tests were performed using custom-built setups. Approximately linear nominal stress–strain profiles were found under tension, while strong strain-stiffening profiles were observed under compression. Low- and high-strain stiffness values were acquired by applying a linear fit to the initial and final 10% of the nominal stress–strain curves. Tensile stiffness values were approximately 15 times higher than low-strain compressive stiffness and 40 times lower than high-strain compressive stiffness values. Tensile stiffness decreased with an increasing RBC volume in the blood mixture. In contrast, high-strain compressive stiffness values increased from 0 to 10%, followed by a decrease from 20 to 80% RBC volumes. Furthermore, inter-donor differences were observed with up to 50% variation in the stiffness of whole blood clot analogues prepared in the same manner between healthy human donors.

Background The purpose of this study was to validate a technique for measuring mean calcium density and to determine associations of cardiovascular risk factors with carotid calcium density. Methods and Results We performed a cross-sectional study in a random sample of 100 stroke-free participants from the population-based Rotterdam Study. The mean calcium density of the combined left and right carotid bifurcations was quantified with a threshold of 130 Hounsfield Units (HU) using a novel density technique. To validate the methodology, carotid calcium volumes acquired using the technique in the current study were compared with measurements computed using dedicated clinical software (semiautomatic technique based on a threshold of ≥130 HU). Next, we investigated the associations of participant demographics, total calcium volume, and known cardiovascular risk factors (hypertension, diabetes, hypercholesterolemia, obesity, and smoking status) with the newly derived mean carotid calcium density measurement using linear regression analyses. Calcium volumes obtained with the 2 methods showed a high agreement (intraclass correlation coefficient=0.99, P<0.001), underlining the validity of the density technique. The total calcium volume was statistically significantly associated with the mean calcium density (cardiovascular risk factors adjusted model (B: 0.48 [95% CI, 0.30-0.66], P<0.001). We also found an association between hypercholesterolemia and mean calcium density (0.46 [0.09-0.83], P=0.017). No other significant associations were found between participant demographics or cardiovascular risk factors and mean carotid calcium density. Conclusions We demonstrated the feasibility of a carotid calcium density measurement technique. The data warrant a subsequent longitudinal study to determine the association between carotid calcium density and the risk of cerebrovascular events.

Background and aims: Atherosclerotic plaque onset and progression are known to be affected by local biomechanical factors. While the role of wall shear stress (WSS) has been studied, the impact of another biomechanical factor, namely mechanical wall stress (MWS), remains poorly understood. In this study, we investigated the association of MWS, independently and combined with WSS, towards atherosclerosis in coronary arteries. Methods: Thirty-four human coronary arteries were analyzed using near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) and optical coherence tomography (OCT) at baseline and after 12 months. Baseline WSS and MWS were calculated using computational models, and wall thickness (ΔWT) and lipid-rich necrotic core size (ΔLRNC) change were measured in non-calcified coronary segments. The arteries were further divided into 1.5 mm/45° sectors and categorized as plaque-free or plaque sectors. For each category, associations between biomechanical factors (WSS & MWS) and changes in coronary wall (ΔWT & ΔLRNC) were studied using linear mixed models. Results: In plaque-free sectors, higher MWS (p < 0.001) was associated with greater vessel wall growth. Plaque sectors demonstrated wall thickness reduction over time, likely due to medical therapy, where higher levels of WSS and WMS, individually and combined, (p < 0.05) were associated with a greater reduction. Sectors with low MWS combined with high WSS demonstrated the highest LRNC increase (p < 0.01). Conclusions: In this study, we investigated the association of the (largely-overlooked) biomechanical factor MWS with coronary atherosclerosis, individually and combined with WSS. Our results demonstrated that both MWS and WSS significantly correlate with atherosclerotic plaque initiation and development.

Rupture of the cap of an atherosclerotic plaque can lead to thrombotic cardiovascular events. It has been suggested, through computational models, that the presence of microcalcifications in the atherosclerotic cap can increase the risk of cap rupture. However, the experimental confirmation of this hypothesis is still lacking. In this study, we have developed a novel tissue-engineered model to mimic the atherosclerotic fibrous cap with microcalcifications and assess the impact of microcalcifications on cap mechanics. First, human carotid plaque caps were analyzed to determine the distribution, size, and density of microcalcifications in real cap tissue. Hydroxyapatite particles with features similar to real cap microcalcifications were used as microcalcification mimics. Injected clusters of hydroxyapatite particles were embedded in a fibrin gel seeded with human myofibroblasts which deposited a native-like collagenous matrix around the particles, during the 21-day culture period. Second harmonic multiphoton microscopy imaging revealed higher local collagen fiber dispersion in regions of hydroxyapatite clusters. Tissue-engineered caps with hydroxyapatite particles demonstrated lower stiffness and ultimate tensile stress than the control group samples under uniaxial tensile loading, suggesting increased rupture risk in atherosclerotic plaques with microcalcifications. This model supports previous computational findings regarding a detrimental role for microcalcifications in cap rupture risk and can further be deployed to elucidate tissue mechanics in pathologies with calcifying soft tissues.

Atherosclerotic plaque rupture in carotid arteries is a major cause of cerebrovascular events. Plaque rupture is the mechanical failure of the heterogeneous fibrous plaque tissue. Local characterization of the tissue's failure properties and the collagen architecture are of great importance to have insights in plaque rupture for clinical event prevention. Previous studies were limited to average rupture properties and global structural characterization, and did not provide the necessary local information. In this study, we assessed the local collagen architecture and failure properties of fibrous plaque tissue, by analyzing 30 tissue strips from 18 carotid plaques. Our study framework entailed second harmonic generation imaging for local collagen orientation and dispersion, and uniaxial tensile testing and digital image correlation for local tissue mechanics. The results showed that 87% of the imaged locations had collagen orientation close to the circumferential direction (0°) of the artery, and substantial dispersion locally. All regions combined, median [Q1:Q3] of the predominant angle measurements was -2° [-16°:16°]. The stretch ratio measurements clearly demonstrated a nonuniform stretch ratio distribution in the tissue under uniaxial loading. The rupture initiation regions had significantly higher stretch ratios (1.26 [1.15-1.40]) than the tissue average stretch ratio (1.11 [1.10-1.16]). No significant difference in collagen direction and dispersion was identified between the rupture regions and the rest of the tissue. The presented study forms an initial step towards gaining better insights into the characterization of local structural and mechanical fingerprints of fibrous plaque tissue in order to aid improved assessment of plaque rupture risk. Statement of significance: Plaque rupture risk assessment, critical to prevent cardiovascular events, requires knowledge on local failure properties and structure of collagenous plaque tissue. Our current knowledge is unfortunately limited to tissue's overall ultimate failure properties with scarce information on collagen architecture. In this study, local failure properties and collagen architecture of fibrous plaque tissue were obtained. We found predominant circumferential alignment of collagen fibers with substantial local dispersion. The tissue showed nonuniform stretch distribution under uniaxial tensile loading, with high stretches at rupture spots. This study highlights the significance of local mechanical and structural assessment for better insights into plaque rupture and the potential use of local stretches as risk marker for plaque rupture for patient-specific clinical applications.

The rupture of atherosclerotic plaques in coronary and carotid arteries is the primary cause of fatal cardiovascular events. However, the rupture mechanics of the heterogeneous, highly collagenous plaque tissue, and how this is related to the tissue's fibrous structure, are not known yet. Existing pipelines to study plaque mechanics are limited to obtaining only gross mechanical characteristics of the plaque tissue, based on the assumption of structural homogeneity of the tissue. However, fibrous plaque tissue is structurally heterogeneous, arguably mainly due to local variation in the collagen fiber architecture. The mechano-imaging pipeline described here has been developed to study the heterogeneous structural and mechanical plaque properties. In this pipeline, the tissue's local collagen architecture is characterized using multiphoton microscopy (MPM) with second-harmonic generation (SHG), and the tissue's failure behavior is characterized under uniaxial tensile testing conditions using digital image correlation (DIC) analysis. This experimental pipeline enables correlation of the local predominant angle and dispersion of collagen fiber orientation, the rupture behavior, and the strain fingerprints of the fibrous plaque tissue. The obtained knowledge is key to better understand, predict, and prevent atherosclerotic plaque rupture events.

Optical coherence elastography (OCE), a functional extension of optical coherence tomography (OCT), visualizes tissue strain to deduce the tissue’s biomechanical properties. In this study, we demonstrate intravascular OCE using a 1.1 mm motorized catheter and a 1.6 MHz Fourier domain mode-locked OCT system. We induced an intraluminal pressure change by varying the infusion rate from the proximal end of the catheter. We analysed the pixel-matched phase change between two different frames to yield the radial strain. Imaging experiments were carried out in a phantom and in human coronary arteries in vitro. At an imaging speed of 3019 frames/s, we were able to capture the dynamic strain. Stiff inclusions in the phantom and calcification in atherosclerotic plaques are associated with low strain values and can be distinguished from the surrounding soft material, which exhibits elevated strain. For the first time, circumferential intravascular OCE images are provided side by side with conventional OCT images, simultaneously mapping both the tissue structure and stiffness.