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In this paper, a two-way fluid-structure coupling model is developed to simulate and analyze the hemodynamic process based on dynamic coronary angiography, and examine the influence of different hemodynamic parameters on coronary arteries in typical coronary stenosis lesions. Using the measured FFR pressure data of a patient, the pressure-time function curve is fitted to ensure the accuracy of the boundary conditions. The average error of the simulation pressure results compared to the test data is 6.74%. In addition, the results related to blood flow, pressure contour and wall shear stress contour in a typical cardiac cycle are obtained by simulation analysis. These results are found to be in good agreement with the laws of the real cardiac cycle, which verifies the rationality of the simulation. In conclusion, based on the modeling and hemodynamic simulation analysis process of dynamic coronary angiography, this paper proposes a method to assist the analysis and evaluation of coronary hemodynamic and functional parameters, which has certain practical significance., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Abstract Background The stenosis of the coronary arteries is usually caused by atherosclerosis. Hemodynamic significance of patient-specific coronary stenoses and the risk of its progression may be assessed by comparing the hemodynamic effects induced by flow disorders. The present study shows how stenosis degree and variable flow conditions in coronary artery affect the oscillating shear index, residence time index, pressure drop coefficient and fractional flow reserve. We assume that changes in the hemodynamic indices in relation to variable flow conditions and geometries evaluated using the computational fluid dynamics may be an additional factor for a non-invasive assessment of the coronary stenosis detected on multi-slice computed tomography. Methods The local-parametrised models of basic shapes of the vessels, such as straight section, bend, and bifurcation as well as the global-patient-specific models of left coronary artery were used for numerical simulation of flow in virtually reconstructed stenotic vessels. Calculations were carried out for vessels both without stenosis, and vessels of 10 to 95% stenosis. The flow rate varied within the range of 20 to 1000 ml/min, and heart rate frequency within the range of 30 to 210 cycles/min. The computational fluid dynamics based on the finite elements method verified by the experimental measurements of the velocity profiles was used to analyse blood flow in the coronary arteries. Results The results confirm our preliminary assumptions. There is significant variation in the coronary hemodynamic indices value caused by disturbed flow through stenosis in relation to variable flow conditions and geometry of vessels. Conclusion Variations of selected hemodynamic indexes induced by change of flow rate, heart rate and vessel geometry, obtained during a non-invasive study, may assist in evaluating the risk of stenosis progression and in carrying out the assessment of the hemodynamic significance of coronary stenosis. However, for a more accurate assessment of the variability of indices and coronary stenosis severity both local (near the narrowing) and global (in side branches) studies should be used.

Tobacco product usage is the single most preventable cause of death in the United States. Smoking promotes atherosclerosis, producing disease in the coronary arteries, the aorta, the carotid and cerebral arteries and the large arteries in the peripheral circulation. The cardiovascular consequences of tobacco products have been the subject of intensive study for several decades. Despite the overwhelming epidemiologic association between smoking and vascular disease, the pathophysiologic mechanisms by which smoking exerts its deleterious effects remain incompletely understood. This review addresses the acute and long-term systemic and coronary hemodynamic effects of tobacco, with an emphasis of the impact on coronary blood flow and pathophysiologic mechanisms., Competing Interests: Disclosure: The author has no conflicts of interest to report., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Recent studies have demonstrated the benefits of using fractional derivatives to simulate a blood pressure profile. In this work we propose to combine a one-dimensional model of coronary blood flow with fractional-order Windkessel boundary conditions. This allows us to obtain a greater variety of blood pressure profiles for better model personalization An algorithm of parameter identification is described, which is used to fit the measured mean value of arterial pressure and estimate the fractional flow reserve (FFR) for a given patient. The proposed framework is used to investigate sensitivity of mean blood pressure and fractional flow reserve to fractional order. We demonstrate that the fractional derivative order significantly affects the fractional flow reserve (FFR), which is used as an indicator of stenosis significance.

Background As younger patients are being considered for transcatheter aortic valve implantation (TAVI), the assessment and treatment of concomitant coronary artery disease is taking on increased importance. Methods and Results Thirteen contemporary lower‐risk patients with TAVI with severe aortic stenosis (AS) and moderate‐severe coronary lesions were included. Patients underwent assessment of coronary hemodynamics in the presence of severe AS (pre‐TAVI), in the absence of severe AS (immediately post‐TAVI), and at longer‐term follow‐up (6 months post‐TAVI). Fractional flow reserve decreased from 0.85 (0.76–0.88) pre‐TAVI to 0.79 (0.74–0.83) post‐TAVI, and then to 0.71 (0.65–0.77) at 6‐month follow‐up (P

Understanding of the mechanisms contributing to the increased maternal susceptibility for major adverse cardiovascular events in the postpartum period remains poor. Accordingly, this study tested the hypothesis that the balance between coronary blood flow and myocardial metabolism is compromised during the puerperium period (35–45 days post-delivery) in swine. Systemic and coronary hemodynamic responses were assessed in anesthetized, open-chest control (nonpregnant) and puerperium/postpartum swine at baseline and in response to intravenous infusion of dobutamine (1–30 μg/kg/min). Blood pressure and heart rate were lower in postpartum swine at baseline and in response to dobutamine (P < 0.05). Coronary blood flow and myocardial oxygen delivery were significantly diminished at baseline in postpartum swine (P < 0.001), which corresponded with ∼35% reduction in myocardial oxygen consumption (MVO 2) (P < 0.001). Postpartum swine displayed enhanced retrograde coronary flow, larger cardiomyocyte area (P < 0.01) and marked capillary rarefaction (P < 0.01). The relationship between coronary blood flow and heart rate (P < 0.05) or MVO 2 (P < 0.001) was significantly diminished in postpartum swine as dobutamine increased MVO 2 up to ∼135% in both groups. This reduction in myocardial perfusion was associated with decreases in myocardial lactate uptake (P < 0.001), increases in coronary venous PCO 2 (P < 0.01) and decreased coronary venous pH (P < 0.01). These findings suggest an impaired balance between coronary blood flow and myocardial metabolism could contribute to the increased incidence of maternal myocardial ischemia and premature death in the postpartum period. [Display omitted] • Alterations in the structure and function of the coronary circulation characterize postpartum changes to the maternal heart. • Resting coronary flow is diminished in the maternal heart in the postpartum condition. • Indices of under-perfusion are present in maternal swine hearts in the postpartum condition. • Mechanisms contributing to dysregulated coronary control in the postpartum maternal heart require further investigation. [ABSTRACT FROM AUTHOR]

Purpose of Review: We aim to summarize the available literature guiding tailored sedation practices for specific conditions encountered in the Cardiovascular Intensive Care Unit (CICU)., Recent Findings: Data specific for the CICU population is lacking. Preclinical data and observational studies guide sedation approaches for specific pathologies that we have used to generate a guideline for sedative choice for various scenarios. We discuss the challenges associated with extubation and highlight the importance of spontaneous breathing trials and role of non invasive ventilation. Understanding the underlying pathology and the effects of sedation and positive pressure ventilation is the base to guide induction and sedation management for patients in the CICU. There is a pressing need for further research to generate high quality clinical data to improve sedation techniques in the CICU., Competing Interests: Declarations. Human and Animal Rights and Informed Consent: This article does not contain any studies with human or animal subjects performed by any of the authors. Competing Interests: The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background and objective: Coronary artery disease (CAD) is highly prevalent and associated with adverse events. Challenges have emerged in the treatment of intermediate coronary artery stenoses. These lesions are often interrogated with fractional flow reserve (FFR) testing to determine if a stenosis is likely to be causative for ischemia in a cardiac territory. This invasive test requires insertion of a pressure wire into a coronary vessel. Recently computational fluid dynamics (CFD) has been used to noninvasively assess fractional flow reserve in vessels reconstructed from medical imaging data. However, many of these simulations are unable to provide additional information about intravascular hemodynamics, including velocity, endothelial shear stress (ESS), and vorticity. We hypothesized that vorticity, which has demonstrated utility in the assessment of ventricular and aortic diseases, would also be an important hemodynamic factor in CAD. Methods: Three-dimensional (3D), patient-specific coronary artery geometries that included all vessels >1mmin diameter were created from angiography data obtained from 10 patients who underwent diagnostic angiography and FFR testing (n = 9). A massively parallel CFD solver (HARVEY) was used to calculate coronary hemodynamic parameters including pressure, velocity, ESS, and vorticity. These simulations were validated by comparing velocity flow fields from simulation to both velocities derived from in vitro particle image velocimetry and to invasively acquired pressure wire-based data from clinical testing. Results: There was strong agreement between findings from CFD simulations and particle image velocimetry experimental testing (ρ < 0.01). CFD-FFR was also highly correlated with invasively measured FFR (ρ = 0.77, p = 0.01) with an average error of 5.9 ± 0.1%. CFD-FFR also had a strong inverse correlation with the vorticity (ρ = -0.86, p = 0.001). Simulations to determine the effect of the coronary stenosis on intravascular hemodynamics demonstrated significant differences in velocity and vorticity (both p < 0.05). Further evaluation of an angiographically normal appearing non-FFR coronary vessel in patients with CAD also demonstrated differences in vorticity when compared with FFR vessels (p < 0.05). Conclusion: The use of highly accurate 3D CFD-derived intravascular hemodynamics provides additional information beyond pressure measurements that can be used to calculate FFR. Vorticity is one parameter that is modified by a coronary stenosis and appears to be abnormal in angiographically normal vessels in patients with CAD, highlighting a possible use-case in preventative screening for early coronary disease. [ABSTRACT FROM AUTHOR]

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Background: Sepsis is a common condition known to impair blood flow regulation and microcirculation, which can ultimately lead to organ dysfunction but such contribution of the coronary circulation remains to be clarified. We investigated coronary blood flow regulatory mechanisms, including autoregulation, metabolic regulation, and endothelial vasodilatory response, in an experimental porcine model of early hyperdynamic sepsis. Methods: Fourteen pigs were randomized to sham (n = 7) or fecal peritonitis-induced sepsis (n = 7) procedures. At baseline, 6 and 12 h after peritonitis induction, the animals underwent general and coronary hemodynamic evaluation, including determination of autoregulatory breakpoint pressure and adenosine-induced maximal coronary vasodilation for coronary flow reserve and hyperemic microvascular resistance calculation. Endothelial-derived vasodilatory response was assessed both in vivo and ex vivo using bradykinin. Coronary arteries were sampled for pathobiological evaluation. Results: Sepsis resulted in a right shift of the autoregulatory breakpoint pressure, decreased coronary blood flow reserve and increased hyperemic microvascular resistance from the 6th h after peritonitis induction. In vivo and ex vivo endothelial vasomotor function was preserved. Sepsis increased coronary arteries expressions of nitric oxide synthases, prostaglandin I2 receptor, and prostaglandin F2α receptor. Conclusion: Autoregulation and metabolic blood flow regulation were both impaired in the coronary circulation during experimental hyperdynamic sepsis, although endothelial vasodilatory response was preserved. [ABSTRACT FROM AUTHOR]

Aortic stenosis (AS) and coronary artery disease (CAD) frequently coexist, with up to two thirds of patients with AS having significant CAD. Given the challenges when both disease states are present, these patients require a tailored approach diagnostically and therapeutically. In this review the authors address the impact of AS and aortic valve replacement (AVR) on coronary hemodynamic status and discuss the assessment of CAD and the role of revascularization in patients with concomitant AS and CAD. Remodeling in AS increases the susceptibility of myocardial ischemia, which can be compounded by concomitant CAD. AVR can improve coronary hemodynamic status and reduce ischemia. Assessment of the significance of coexisting CAD can be done using noninvasive and invasive metrics. Revascularization in patients undergoing AVR can benefit certain patients in whom CAD is either prognostically or symptomatically important. Identifying this cohort of patients is challenging and as yet incomplete. Patients with dual pathology present a diagnostic and therapeutic challenge; both AS and CAD affect coronary hemodynamic status, they provoke similar symptoms, and their respective treatments can have an impact on both diseases. Decisions regarding coronary revascularization should be based on understanding this complex relationship, using appropriate coronary assessment and consensus within a multidisciplinary team. [Display omitted] • The coexistence of epicardial CAD among patients with AS is common. • Diagnostic and treatment alternatives remain ambiguous and highly debated. • Physiological changes of AS on hemodynamic status challenge assessment of concomitant CAD. • Studies evaluating the efficacy of revascularization in patients with AS are needed. [ABSTRACT FROM AUTHOR]

Background: Current diagnostic criteria for coronary spasm are based on patient's symptoms, ECG shifts and epicardial vasoconstriction during acetylcholine (ACh) spasm testing. Aims: To assess the feasibility and diagnostic value of coronary blood flow (CBF) and resistance (CR) assessment as objective parameters during ACh testing. Methods: Eighty-nine patients who underwent intracoronary reactivity testing including ACh testing with synchronous Doppler wire-based measurements of CBF and CR were included. Coronary microvascular and epicardial spasm, respectively, were diagnosed based on COVADIS criteria. Results: Patients were 63 ± 13 years old, predominantly female (69%) and had preserved LV ejection fraction (64 ± 8%). Overall, assessment of CBF and CR during ACh testing revealed a decrease in CBF of 0.62 (0.17–1.53)-fold and an increase of CR of 1.45 [0.67–4.02]-fold in spasm patients compared to 2.08 (1.73–4.76) for CBF and 0.45 (0.44–0.63) for CR in patients without coronary spasm (both p < 0.01). Receiver operating characteristic revealed a high diagnostic ability of CBF and CR (AUC 0.86, p < 0.001, respectively) in identifying patients with coronary spasm. However, in 21% of patients with epicardial spasm and 42% of patients with microvascular spasm a paradoxical response was observed. Conclusions: This study demonstrates feasibility and potential diagnostic value of intracoronary physiology assessments during ACh testing. We observed opposite responses of CBF and CR to ACh in patients with positive vs. negative spasm test. While a decrease in CBF and an increase in CR during ACh seem pathognomonic for spasm, some patients with coronary spasm demonstrate paradoxical ACh response demanding further scientific investigations. [ABSTRACT FROM AUTHOR]

Purpose: It is difficult for doctors to decide whether patients with suspected coronary heart disease classified as Coronary Artery Disease Reporting and Data System (CAD-RADS) < 3 should be administered preventive treatment, or whether non-atherosclerotic chest pain should be considered. The aim of the current study was to investigate coronary hemodynamic characteristics in such patients, which may provide more information on their stenosis and be helpful for initial diagnoses. Methods: Two patient-specific models were reconstructed based on the coronary computed tomographic angiography underwent in 2012. Patient 1 was classified as CAD-RADS 0, and was readmitted to hospital due to coronary artery disease within 5 years. Patient 2 was classified as CAD-RADS 2, and has experienced no adverse events to date. Computational fluid dynamics (CFD) analysis was used to obtain hemodynamic parameters including flow rate waveform, flow streamlines, time-average wall shear stress (TAWSS), and oscillatory shear index (OSI). Results: Patient 1 exhibited no physiological characteristics of right coronary artery flow waveform, large areas of low TAWSS, and slow blood flow in the proximal and middle segments of the left anterior descending branch. Patient 2 exhibited reduced coronary supply, small and separate areas of abnormal TAWSS, and a higher left anterior descending branch OSI than patient 1. Conclusion: Hemodynamic abnormalities may play an important role in the prognosis of patients with coronary stenosis, and patient-specific hemodynamic characteristics may facilitate more accurate initial diagnosis, and better management. Overall hemodynamics (along the whole vessel) warranted attention at the time of the initial visit in patients classified as CAD-RADS < 3. [ABSTRACT FROM AUTHOR]

Background: Coronary chronic total occlusion (CTO) is characterized by the presence of collateral blood vessels which can provide additional blood supply to CTO-artery dependent myocardium. Successful CTO recanalization is followed by significant decrease in collateral donor artery blood flow and collateral derecruitment, but data on coronary hemodynamic changes in relation to myocardial function are limited. We assessed changes in coronary flow velocity reserve (CFVR) by echocardiography in collateral donor and recanalized artery following successful opening of coronary CTO.Methods: Our study enrolled 31 patients (60 ± 9 years; 22 male) with CTO and viable myocardium by SPECT scheduled for percutaneous coronary intervention (PCI). Non-invasive CFVR was measured in collateral donor artery before PCI, 24 h and 6 months post-PCI, and 24 h and 6 months in recanalized artery following successful PCI of CTO.Results: Collateral donor artery showed significant increase in CFVR 24 h after CTO recanalization compared to pre-PCI values (2.30 ± 0.49 vs. 2.71 ± 0.45, p = 0.005), which remained unchanged after 6-months (2.68 ± 0.24). Baseline blood flow velocity of the collateral donor artery significantly decreased 24 h post-PCI compared to pre-PCI (0.28 ± 0.06 vs. 0.24 ± 0.04 m/s), and remained similar after 6 months, with no significant difference in maximum hyperemic blood flow velocity pre-PCI, 24 h and 6 months post-PCI. CFVR of the recanalized coronary artery 24 h post-PCI was 2.55 ± 0.35, and remained similar 6 months later (2.62 ± 0.26, p = NS).Conclusions: In patients with viable myocardium, prompt and significant CFVR increase in both recanalized and collateral donor artery, was observed within 24 h after successful recanalization of CTO artery, which maintained constant during the 6 months.Trial Registration: ClinicalTrials.gov (Number NCT04060615 ). [ABSTRACT FROM AUTHOR]

Coronary arteries serve a crucial purpose in the circulatory system as they supply blood to the human heart, a highly oxidative organ. As the blood flows through these arteries, the constituents of blood such as proteins and fatty acid molecules may start depositing on the arterial lining. These depositions narrow down the arteries and obstruct the blood flow to the heart. This phenomenon is termed as atherosclerosis, responsible for coronary artery disease, a leading cause of death globally. The progression of disease is affected by coronary hemodynamics which strongly depends on the geometrical complexities such as branching and tapering, and the associated parameters such as curvature and tortuosity. These geometrical parameters vary across the population and are affected by factors such as dietary habits, gender, lifestyle and genetics. Technological advancements in the past few decades have resulted in emergence of patient-specific computational fluid dynamics (CFD) modelling as an important tool in cardiovascular engineering and technology. Patient-specific CFD modelling utilises the clinically obtained patient-specific geometrical and boundary condition data to model the flow and gain an insight in the detailed hemodynamic behaviour, calculate different parameters which can be used as biomarkers and assess different treatment options. In this article, we provide a brief overview of the human coronary circulation and typical steps involved in patient-specific modelling. Further, the studies on patient-specific coronary hemodynamics are extensively reviewed and a perspective on future trends is provided. We believe that the article will serve as a beginner's guide for the researchers working in this emerging area. [ABSTRACT FROM AUTHOR]

Patients with anomalous coronary artery origins (AOCA) exhibit a higher risk of atherosclerosis, where even minimal stenosis may lead to adverse cardiovascular events. However, the factors contributing to this heightened risk in AOCA patients remain unclear. This study aimed to investigate whether an AOCA patient is more prone to stenosis occurrence and its progression in view of hemodynamics. A patient whose left circumflex artery originated from the right coronary sinus with a mild stenosis in the left anterior descending (LAD) artery and a healthy individual were included in this study. Two additional models were developed by removing stenosis from the patient model and adding a corresponding stenosis to the healthy model. Additionally, the inlet flow waveforms for the left and right coronary arteries were swapped in both the patient and healthy models. Results indicated that the AOCA patient without stenosis demonstrated higher wall pressure (LAD: 95.57 ± 0.73 vs. 93.86 ± 0.50 mmHg; LCX: 94.97 ± 0.98 vs. 93.47 ± 0.56 mmHg; RCA: 96.23 ± 0.30 vs. 93.86 ± 0.46 mmHg) and TAWSS (LAD: 24.41 ± 19.53 vs. 13.82 ± 9.87 dyne/cm2, p < 0.0001; LCX: 27.21 ± 14.51 vs. 19.33 ± 8.78 dyne/cm2) compared to the healthy individual, with similar trends also observed in stenotic conditions. Significant changes in the LCX flow distribution were also noted under varying pulsatile conditions (LCX: 18.28% vs. 9.16%) compared to the healthy individual. The high-pressure, high-shear hemodynamic environment in AOCA patients predisposes them to atherosclerosis, and the unique geometry exacerbates hemodynamic abnormalities when stenosis occurs. Clinicians should closely monitor AOCA patients with stenosis to prevent adverse cardiovascular events. [ABSTRACT FROM AUTHOR]

Background: High-density lipoprotein (HDL) protects against myocardial ischemia-reperfusion (I/R) injury. Mammalian target of rapamycin complexes 1 and 2 (mTORC1 and mTORC2) play opposing roles in protecting against I/R injury, whereby mTORC1 appears to be detrimental while mTORC2 is protective. However, the role of HDL and mTORC signaling in protecting against I/R in hypertensive rodents is not clearly understood. In this study, we investigated the involvement of mTORC1 and mTORC2 in HDL-mediated protection against myocardial I/R injury in normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Methods: Hearts from WKY and SHR were subjected to I/R injury using a modified Langendorff system. Hemodynamics data were collected, and infarct size was measured. Rapamycin and JR-AB2-011 were used to test the role of mTORC1 and mTORC2, respectively. MK-2206 was used to test the role of Akt in HDL-mediated cardiac protection. The expression levels and the activation states of mediators of mTORC1 and mTORC2 signaling and myocardial apoptosis were measured by immunoblotting and/or enzyme-linked immunosorbent assay (ELISA). Results: HDL protected hearts from WKY and SHR against I/R injury as indicated by significant improvements in cardiac hemodynamics and reduction in infarct size. HDL induced greater protection in WKY compared to SHR. HDL treatment attenuated mTORC1 signaling in WKY by reducing the phosphorylation of P70S6K (mTORC1 substrate). In SHR however, HDL attenuated mTORC1 signaling by reducing the levels of phospho-mTORC1, Rag C (mTORC1 activator), and phospho-PRAS40 (mTORC1 inhibitor). HDL increased the phosphorylation of mTORC2 substrate Akt, specifically the Akt2 isoform in SHR and to a greater extent in WKY. HDL-induced protection was abolished in the presence of Akt antagonist and involved attenuation of GSK, caspases 7 and 8 activation, and cytochrome C release. Conclusion: HDL mediates cardiac protection via attenuation of mTORC1, activation of mTORC2-Akt2, and inhibition of myocardial apoptosis. HDL regulates mTORC1 and mTORC2 signaling via distinct mechanisms in normotensive and hypertensive rats. HDL attenuation of mTORC1 and activation of mTORC2-Akt2 signaling could be a mechanism by which HDL protects against myocardial I/R injury in hypertension. [ABSTRACT FROM AUTHOR]

As the current guidelines on myocardial revascularization recommend, transit-time flow measurement (TTFM) is increasingly used for intraoperative graft flow analysis during coronary artery bypass grafting (CABG) as a less invasive, more highly reproducible, and less time-consuming method. In addition to the morphological assessment using color Doppler, mean graft flow (Qm) > 15 ml/min, pulsatility index (PI) < 5.0, diastolic filling (DF) > 50%, and systolic reverse flow (SRF) < 4% have been reported to predict patent CABG grafts. However, it is difficult to determine the clear-cut cut-off value of these parameters, because they varies with the hemodynamic characters, including fractional flow reserve (FFR) of the target coronary artery. In addition to these parameters, we focused on fast Fourier transform (FFT) analysis, because the TTFM waveform morphology may be more important than Qm itself. FFT analysis is based on the principle that any periodic waveforms can be broken down into a series of pure sine waves or harmonics. Herein we review FFT analysis of the intraoperative TTFM waveforms for quality assessment of CABG grafts. [ABSTRACT FROM AUTHOR]

Purpose: Numerical models that simulate the behaviors of the coronary arteries have been greatly improved by the addition of fluid-structure interaction (FSI) methods. Although computationally demanding, FSI models account for the movement of the arterial wall and more adequately describe the biomechanical conditions at and within the arterial wall. This offers greater physiological relevance over Computational Fluid Dynamics (CFD) models, which assume the walls do not move or deform. Numerical simulations of patient-specific cases have been greatly bolstered by the use of imaging modalities such as Computed Tomography Angiography (CTA), Magnetic Resonance Imaging (MRI), Optical Coherence Tomography (OCT), and Intravascular Ultrasound (IVUS) to reconstruct accurate 2D and 3D representations of artery geometries. The goal of this study was to conduct a comprehensive review on CFD and FSI models on coronary arteries, and evaluate their translational potential. Methods: This paper reviewed recent work on patient-specific numerical simulations of coronary arteries that describe the biomechanical conditions associated with atherosclerosis using CFD and FSI models. Imaging modality for geometry collection and clinical applications were also discussed. Results: Numerical models using CFD and FSI approaches are commonly used to study biomechanics within the vasculature. At high temporal and spatial resolution (compared to most cardiac imaging modalities), these numerical models can generate large amount of biomechanics data. Conclusions: Physiologically relevant FSI models can more accurately describe atherosclerosis pathogenesis, and help to translate biomechanical assessment to clinical evaluation. [ABSTRACT FROM AUTHOR]

Early revascularization for patients with acute myocardial infarction (AMI) is of outmost importance in limiting infarct size and associated complications, as well as for improving long-term survival and outcomes. However, reperfusion itself may further damage the myocardium and increase the infarct size, a condition commonly recognized as myocardial reperfusion injury. Several strategies have been developed for limiting the associated with reperfusion myocardial damage, including hypothermia. Hypothermia has been shown to limit the degree of infarct size increase, when started before reperfusion, in several animal models. Systemic hypothermia, however, failed to show any benefit, due to adverse events and potentially insufficient myocardial cooling. Recently, the novel technique of intracoronary selective hypothermia is being tested, with preclinical and clinical results being of particular interest. Therefore, in this review, we will describe the pathophysiology of myocardial reperfusion injury and the cardioprotective mechanics of hypothermia, report the animal and clinical evidence in both systemic and selective hypothermia and discuss the potential future directions and clinical perspectives in the context of cardioprotection for myocardial reperfusion injury. [ABSTRACT FROM AUTHOR]