Coronary artery bypass grafting (CABG) is the first-line therapy for 90% coronary artery stenosis, yet conventional hemodynamic simulations of CABG ignore the microcirculation system, leading to a lack of physiological condition. In this work, we construct numerical models of one-way/two-way arterial bypass with 20 degrees, 30 degrees and 45 degrees anastomotic angles for 90% stenosis, integrate microcirculation as a seepage outlet via porous media, and adopt two-way fluid-structure interaction (FSI) to assess key hemodynamic and structural parameters across representative cross-sections. The results show that the 30 degrees anastomotic angle outperforms 20 degrees and 45 degrees in both configurations, and the two-way bypass exhibits superior hemodynamic performance compared to one-way bypass, with the 30 degrees two-way bypass model achieving the most stable structural response and optimal local hemodynamic microenvironment. This study reveals the optimal CABG design parameters under microcirculatory regulation, offering a hemodynamic theoretical basis for individualized CABG surgical planning and preoperative decision-making in cardiovascular clinical practice.

Pulmonary artery stenosis is closely related to hemodynamics. The effects of porosity on hemodynamics in pulmonary artery stenosis are investigated in this work. A real human pulmonary artery stenosis model is established and the computational domain is formed according to CT images of the right lower pulmonary artery. The stenosis is simulated by porous media, and the fluid-structure coupling method is used, considering the effects of different porosities on quantitative pulmonary pressure ratio (QPPR) and hemodynamics of pulmonary artery stenosis. The inlet velocity and the outlet pressure are given. On the interface of fluid-solid coupling, it is assumed that the motions of the fluid and wall are the same, and there is no sliding. The results show that QPPR is, respectively, 0.5812, 0.6556, and 0.6606 under the 0.3, 0.5, 0.8 porosities. This study proves that porosity has a great influence on the QPPR and hemodynamics of stenosed artery, and it is a non-negligible factor. The numerical results of this paper provide a potential theoretical basis for the diagnosis and treatment of pulmonary stenosis.

BackgroundIn recent years, for patients with arterial stenosis up to 75% and poor medical control, stent implantation has become the mainstream choice.ObjectiveThe purpose of this work is to study the effects of stent implantation on hemodynamics in the stenotic artery considering microcirculation.MethodsA stent implantation model with microcirculation is constructed. Expansion simulations are carried out for the grid stent and the link stent respectively to analyze the changes in hemodynamic parameters and the mechanical responses of the plaque and the stent.ResultsCompared with the stent implantation study without microcirculation, the results show that the pressure gradient decreases, and the probability of high time averaged wall shear stress near the stent wires reduces after the grid stent is implanted and expanded. The link stent generates time averaged wall shear stress close to the normal physiological range, and no regions with high oscillatory shear index and high relative residence time are found near the stent wire upstream of the stent.ConclusionsThe link stent can not only better improve the hemodynamic environment, but also reduce the risk of intimal hyperplasia and atherosclerosis. These findings reflect the importance of microcirculation in the regulation of hemodynamics after different stent implantations, providing a new perspective for optimizing stent design.

Atherosclerosis is prone to occur at arterial bifurcations. The hemodynamic and biomechanical variations across subtypes of Chen’s bifurcation lesion classification are still unclear. This study adopts bidirectional fluid–structure interaction simulations to explore biomechanical features of four common Chen-classified lesion subtypes ([Formula: see text], [Formula: see text], [Formula: see text], [Formula: see text] in 60% stenotic bifurcated arteries with unstable plaques. The assumptions of the idealized models and the finite volume computational fluid dynamics technique are used. Multiple hemodynamic and biomechanical indicators are calculated, and plaque fatigue life is evaluated via Basquin S–N curve and Palmgren–Miner rule. The results reveal significant inter-subtype differences in hemodynamic and mechanical properties. Type [Formula: see text] presents elevated wall shear stress and oscillatory shear index at the bifurcation ridge alongside the longest fatigue life. Types [Formula: see text] and [Formula: see text] have a short fatigue life owing to drastic stress fluctuations. Type [Formula: see text] possesses the highest flow velocity and time-averaged wall shear stress with obvious turbulence at the branch inlets. Bifurcation ridges and proximal plaque shoulders are identified as high-risk vulnerable regions. This work offers biomechanical references for risk assessment and targeted therapy of bifurcation lesions.

BACKGROUND:Understanding metabolic evolution of right ventricle (RV) of pulmonary arterial hypertension associated with atrial septal defect (PAH-ASD) helps elucidate the underlying pathobiology and reveal disease-specific biomarkers. However, the exact metabolic profile of RV of PAH-ASD is scarce. OBJECTIVES:This study aimed to unveil precisely the metabolic signatures of trans-RV of PAH-ASD through non-targeted metabolomics. METHODS:Participants with PAH-ASD were recruited and their blood samples were obtained from superior vena cava (SVC) and pulmonary artery (PA) through right cardiac catheterization. Non-targeted metabolomics analysis on the basis of UHPLC-MS/MS was utilized to generate the metabolomic signature of trans-RV by comparing the metabolites change from SVC to PA. RESULTS:1060 metabolites were detected from blood samples from 40 PAH-ASD participants. A total of 44 differential metabolites were identified based on screening criteria after flowing through the RH, including 10 metabolites with decreased levels and 34 metabolites with increased levels. Among them, phosphatidylcholines, sphingomyelins, AICARP, XMP, inosine 5'-Monophosphate, prostaglandin A1, oleoyl ethanolamide, tyramine, 2-phenylethylamine, 23-nordeoxycholic acid, LPI 20:4, and LPE 22:6 were discovered. Moreover, distinct metabolic perturbations, such as the change of sphingomyelins, inosine 5'-Monophosphate and LPE 22:6, was correlated with the significant clinical variables indicating RV dysfunction in clinical association analysis. CONCLUSION:Our study correctly defined metabolic signatures indicating towards a metabolic pathogenesis of trans-RV of PAH-ASD, emphasizing the importance of these metabolites in promoting of RV dysfunction and devising therapeutic strategies.

Background: The Platelet-to-HDL-cholesterol ratio (PHR), an emerging inflammatory biomarker, shows promise as a predictor in patients with type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD). However, the association between PHR and glycemic metabolism status and their combined effects on the prognosis of CAD patients undergoing percutaneous coronary intervention (PCI) remains unclear. Methods: A total of 31,761 CAD patients hospitalized for PCI were included. The primary endpoint was defined as major adverse cardiovascular events (MACEs). According to the median PHR levels, patients were grouped into higher levels of PHR (PHR-H) and lower levels of PHR (PHR-L) and further divided by glycemic status into four groups: PHR-H/T2DM, PHR-H/Non-T2DM, PHR-L/T2DM, PHR-L/Non-T2DM. Results: During the 1-year follow-up, 2258 (7.1%) MACEs occurred. Elevated PHR conferred 17% excess risk for MACEs. A 1-unit increase in LnPHR was associated with a 26% increased risk of MACEs in the T2DM cohort, and a 27% increase of MACEs risks in the non-T2DM cohort. Compared to those in PHR-H/T2DM group, patients in PHR-L/T2DM, PHR-H/Non-T2DM, PHR-L/Non-T2DM had significantly decreased risk of MACEs [adjusted hazard ratio (aHR): 0.83, 95% confidence interval (CI): 0.73- 0.96, P =0.009; aHR: 0.81, 95% CI: 0.69- 0.95, P =0.009; aHR: 0.70, 95% CI: 0.60- 0.83, P < 0.001; respectively]. Cox regression analysis also indicated the highest risk of MACEs among patients in PHR-H/T2DM group than in other groups (P for trend < 0.001). Restricted cubic spline analyses revealed positive linear associations of PHR with MACEs, all-cause death, and unplanned target vessel revascularization, while a significant non-linear relationship between PHR and myocardial infarction. Additionally, subgroup analysis indicated consistent effects on MACEs within diverse subsets. Conclusion: Elevated PHR levels combined with T2DM were associated with worse clinical outcomes after PCI at 1-year follow-up. The PHR may serve as a valuable predictor for identifying high-risk patients post-PCI, particularly in diabetic cohorts.

Cardiovascular-kidney-metabolic (CKM) syndrome stages 0–3 represent a critical window for preventing progression to overt cardiovascular disease (CVD). Insulin resistance (IR) is central to CKM pathophysiology, yet the comparative utility of longitudinal IR patterns (cumulative burden and longitudinal pattern groups) across multiple surrogates, and the mediating role of biological ageing, remain unexamined in this preclinical population. We included 3948 participants with CKM stages 0–3 from the CHARLS 2011–2020. Twelve IR surrogates (TyG and derivatives, METS-IR, CTI, eGDR, TG/HDL-C) were assessed via cumulative exposure and K-means-derived pattern groups. Associations with incident CVD were evaluated using Fine-Gray competing risk models, spline regression, receiver operating characteristic analyses, and quantile-based models. Mediation analyses quantified the contribution of biological age acceleration. 756 (19.1

Coronary artery ectasia (CAE), a rare pathological entity characterized by pathological coronary dilation, frequently coexists with coronary artery disease (CAD). Emerging evidence implicates insulin resistance (IR) in atherosclerotic progression, with the triglyceride–glucose (TyG) index—a validated IR surrogate—being clinically associated with CAD severity. However, its relationship with multi-vessel CAD in CAE populations remains underexplored. This cross-sectional study analyzed 585 CAE patients with CAD undergoing percutaneous coronary intervention (PCI) at Fuwai Hospital (2016–2018). Participants were stratified by TyG index (low/high) and CAD severity (single/multi-vessel CAD). Multivariable-adjusted logistic regression was used to evaluate the association between the TyG index and multi-vessel CAD. Restricted cubic splines (RCS) were applied to assess dose–response relationships. Incremental predictive value was quantified via C-statistics, net reclassification improvement (NRI), and integrated discrimination improvement (IDI) relative to baseline risk models. The study population had a mean age of 58.1 ± 10.6 years, and 496 (84.8

INTRODUCTION:Right heart (RH), as a junction between the venous system and pulmonary circulation, gains great emphasis on exploring the relevant pathological mechanism of many cardiopulmonary diseases. Although these pathogensis researches centering on RH-related diseases advance, the physiological mechanism research of the RH is scarce. OBJECTIVES:This study aimed to accurately unravel the metabolic features of normal trans-RH through non-targeted metabolomics. METHODS:Patent foramen ovale (PFO) participants with normal function of RH were recruited and their blood samples from superior vena cava (SVC) and pulmonary artery (PA) were collected through right cardiac catheterization. Non-targeted metabolomics analysis based on UHPLC-MS/MS was utilized to generate the metabolic feature of trans-RH by comparing the metabolites change from SVC to PA, revealing its physiological gradient metabolic mechanism. RESULTS:1060 metabolites were tentatively identified in blood samples from 28 PFO participants. 51 differential metabolites were defined based on screening criteria after flowing through RH, including 39 down-regulated metabolites and 12 up-regulated metabolites. Among them, phosphatidylcholines, sphingomyelins, amino acids, triacylglycerol, neopterin, and tetradecanedioic acid were the most relevant. CONCLUSION:Our study provides a more profound and extensive understanding of the psychological metabolism of trans-RH, expanding the current knowledge of normal RH function and providing clues for the pathogenesis research of RH-related diseases.

The aim of this study was to evaluate and compare the usefulness of the C-reactive protein (CRP)-triglyceride glucose (TyG) index (CTI) and other insulin resistance (IR) or inflammatory indexes for predicting recurrent cardiovascular events in percutaneous coronary intervention (PCI)—treated patients. In addition, the mediating effects of systemic inflammation, represented by high-sensitive CRP (hs-CRP), on TyG index-associated adverse cardiovascular events across different subgroups were also evaluated. The formula for calculating the CTI was 0.412 × ln [high-sensitivity CRP (mg/L)] + ln [triglyceride (mg/dl) × fasting glucose (mg/dl)/2]. The primary endpoint was defined as the incidence of major adverse cerebrovascular and cardiovascular events (MACCEs), including cardiovascular death, nonfatal acute myocardial infarction (AMI), nonfatal ischemic stroke and repeat coronary revascularization. Among the 2383 PCI-treated patients, 413 experienced MACCEs during a median of 34 months follow-up. Correlation analysis showed CTI was significantly associated with cardiometabolic factors. The CTI was the strongest predictor for MACCEs (adjusted HR 1.85, 95

Early identification of patients at risk of acute coronary syndrome (ACS) remains a major unmet need, particularly among those with stable coronary artery disease (sCAD), where timely intervention could markedly improve outcomes. The gut microbiota has been implicated in coronary artery disease (CAD), but its ability to distinguish ACS from sCAD is not well defined. Here, we performed cross-sectional multi-omics profiling of fecal microbiota and plasma metabolites in 548 individuals, including participants with normal coronary arteries (N = 175), primary sCAD (N = 161), and ACS (N = 212). To assess whether disease-associated changes resolve with treatment, we further analyzed an independent cohort of ACS patients (N = 52) who transitioned to sCAD following standard therapy. We identified profound ACS-associated alterations in gut microbial composition and systemic metabolism, marked by enrichment of pro-inflammatory taxa such as Streptococcus spp. and elevated circulating levels of 3-hydroxybutyrate (3-HB). Strikingly, many of these ACS-specific microbial and metabolic signatures, including 3-HB and related microbial functional pathways, were restored toward sCAD-like levels after clinical recovery. Integrative models combining microbial taxa, metabolites, and clinical biomarkers robustly discriminated ACS from healthy controls (AUC = 0.91) and from sCAD (AUC = 0.83), significantly outperforming clinical markers alone (AUC = 0.69 for NCA vs. ACS; 0.59 for sCAD vs. ACS). These findings establish the gut microbiome and its metabolic outputs as key discriminators of ACS, reveal their dynamic resolution during disease recovery, and highlight their potential as biomarkers and therapeutic targets for cardiovascular risk stratification and management.

Background: The applicability of currently established high-risk inflammatory criteria to East Asian patients is unknown, particularly concerning the hypersensitive C-reactive protein (hs-CRP) cutoff value. In addition, the role of cholesterol and inflammation in determining the prognosis of these patients might shift after the patient accepts lipid-lowering treatments. This study aimed to explore the high-risk hs-CRP cutoff value and compare the prognostic value between inflammation and cholesterol risk in the East Asian population after treatment with percutaneous coronary intervention (PCI). Methods: Post-PCI patients with serial hs-CRP and low-density lipoprotein cholesterol (LDL-C) level measurements were retrospectively enrolled. Major adverse cardiovascular and cerebrovascular events (MACCEs) were defined as a composite of cardiovascular death, non-fatal acute myocardial infarction (AMI), non-fatal stroke, and unplanned coronary revascularization. The association between residual risks and MACCEs was evaluated. Results: During a median follow-up of 30.4 months, 403 MACCEs occurred among 2373 patients. The high-risk LDL-C and hs-CRP cutoff values in the present study were set at 1.56 mg/L and 1.80 mmol/L, respectively, based on the results of tertile stratification and restricted cubic spline analysis. The adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) of residual cholesterol risk (hs-CRP <1.56 mg/L; LDL-C ≥1.80 mmol/L), residual inflammatory risk (hs-CRP ≥1.56 mg/L; LDL-C <1.80 mmol/L), and residual cholesterol and inflammatory risk (hs-CRP ≥1.56 mg/L; LDL-C ≥1.80 mmol/L) for MACCEs were 1.26 (0.95–1.66), 2.15 (1.57–2.93), and 2.07 (1.55–2.76), respectively. Inflammatory-induced MACCEs were more likely to be associated with the increased risk of non-fatal AMI (HR: 4.48; 95% CI: 2.07–9.73; p < 0.001), while cholesterol-induced MACCEs were more likely to be associated with the increased risk of non-target vessel revascularization (TVR: HR: 1.60; 95% CI: 1.08–2.37; p = 0.019). Persistent high inflammatory risk (baseline and follow-up hs-CRP ≥1.56 mg/L) can be a major determinant of MACCEs (adjusted HR: 2.03; 95% CI: 1.64–2.52; p < 0.001), while persistent high cholesterol risk (baseline and follow-up LDL-C ≥1.80 mmol/L) was not. Serial hs-CRP measurements could produce more predictive values for MACCEs than a single measurement. Conclusions: Despite statin treatment, residual cholesterol and inflammatory risks persist in post-PCI patients. The high-risk hs-CRP standard may be lower in East Asian patients than their Western counterparts, with a cutoff value of 1.56 mg/L. Inflammation and cholesterol could be major determinants for recurrent cardiovascular events, while hs-CRP seems to be a stronger predictor than LDL-C in post-PCI patients receiving statin therapy. Clinical Trial Registration: ChiCTR2100047090, https://www.chictr.org.cn/showproj.html?proj=127821.

BACKGROUND:In heart failure with preserved ejection fraction (HFpEF), elevated mean left atrial pressure (MLAP) is a recognised haemodynamic feature. This pilot study explored the use of a personalised approach-combined radiofrequency ablation and balloon dilation (CURB)-to establish interatrial communication in patients with elevated resting MLAP. METHODS:Between September 2020 and March 2023, a single-arm study was conducted at Fuwai Hospital (Beijing, China) in patients with HFpEF and resting MLAP ≥18 mm Hg. CURB was performed using graded balloon dilation to achieve an MLAP target of <15 mm Hg, followed by rim stabilisation with radiofrequency ablation. Clinical status, interatrial fenestration and haemodynamic parameters were assessed during follow-up. RESULTS:Thirty-two patients were included (mean age 68.4 years; 59% male). The procedural target was achieved in 31 patients (97%). Median MLAP changed from 19.0 mm Hg (IQR 18.0, 21.0) to 13.0 mm Hg (IQR 12.0, 13.3), and mean pulmonary arterial pressure from 26.9 mm Hg (SD 3.9) to 23.5 mm Hg (SD 3.7). Over a median follow-up of 15.5 months (IQR 11.0, 18.0), fenestrations remained patent. The intervention was associated with favourable change in New York Heart Association functional class (median change: -1 class), 6 min walk distance (+48.5 m) and quality of life scores (-21.7 points). Reassessment in a subset (n=8) beyond 1 year showed sustained MLAP levels. CONCLUSIONS:Among patients with HFpEF and elevated MLAP, the CURB technique was feasible and associated with mid-term changes in haemodynamics and functional measures. Further controlled studies are needed to assess long-term outcomes, safety and broader applicability. TRIAL REGISTRATION NUMBER:NCT04573166.

Residual chronic obstruction of Pulmonary Embolism (PE) can contribute to pulmonary hypertension and persistent cardiopulmonary limitations. This study comprehensively investigates the influence factors on the resolution of PE clots by CT pulmonary angiography (CTPA). A retrospective analysis of 102 patients with acute PE diagnosed by CTPA was conducted based on a registered prospective PE cohort (NCT06073366). Follow-up CTPA studies (3 to 6 months post-diagnosis) were analyzed for the rate of improvement and the complete resolution rate of PE clots. Univariate analyses were performed using chi-square tests, and multivariate logistic regression was applied to adjust for confounding factors. A total of 2,958 vessels from 102 participants were analyzed, 219 were completely obstructed, and 1439 were partially obstructed. We did not identify any factors that had a significant effect on the rate of improvement. The complete resolution rate of PE clots was lower in completely obstructed vessels compared to partially obstructed vessels, and they had a 110

INTRODUCTION:Direct oral anticoagulants (DOACs) are increasingly prescribed for life-long anticoagulation in chronic thromboembolic pulmonary hypertension (CTEPH) patients, despite not being recommended in the guidelines. This study aims to evaluate the efficacy and safety of DOACs in CTEPH patients. METHODS:From May 2013 to December 2022, patients who were first diagnosed with CTEPH in Fuwai Hospital and started long-term anticoagulation treatment with warfarin or DOACs were retrospectively included and followed up until (1) death, (2) transition to other kinds of anticoagulants, or (3) discontinuation of anticoagulation. Propensity score matching was used to balance confounding bias of baseline characteristics. All-cause death, major bleeding, clinically relevant nonmajor bleeding and venous thromboembolism (VTE) recurrence were obtained and analysed. RESULTS:After propensity score matching, 115 patients taking warfarin and 206 patients taking DOACs were included in our study and followed up for 5.5 [3.4, 7.1] years. There was no significant difference of survival between the warfarin and the DOAC group (p = 0.77). The exposure adjusted event rate of major bleeding (0.3 %/person-year vs 0.4 %/person-year, p = 0.705) and clinically relevant nonmajor bleeding (3.1 %/person-year vs 3.2 %/person-year, p > 0.999) was similar between two groups. The exposure adjusted rate of VTE recurrence was significantly higher in the DOAC group (1.5 %/person-year vs 0.3 %/person-year, p = 0.030). CONCLUSION:In anticoagulation of CTEPH patients, DOACs have similar survival rate, similar risk of bleeding but higher risk of VTE recurrence than warfarin.

Background Inflammation and insulin resistance play important roles in the initiation and progression of heart failure and coronary artery disease. However, there’s lack of indicator related to inflammation and insulin resistance to predict the prognosis of that population. This study aims to evaluate the potential value of C-reactive protein-triglyceride glucose index (CTI) in heart failure patients undergoing percutaneous coronary intervention (PCI). Methods 2797 PCI-treated patients with heart failure at Beijing Fuwai Hospital between 1st January 2016 and 31st December 2018 were retrospectively enrolled in current study. The primary endpoint was major adverse cardiac and cerebrovascular events at 12-month follow-up, defined as a composite of all-cause death, non-fatal myocardial infarction and stroke. Restricted cubic spline was applied to determine the cut-off value of CTI and examine the dose-response relationship between the CTI and the primary endpoint. Multivariate Cox proportional hazards models were used to evaluate the predictive value of CTI for the adverse cardiovascular outcomes and the results were expressed as hazard ratio with 95% confidence interval. The receiver-operating characteristics and decision curve analysis were plotted to comprehensively evaluate the predictive accuracy and clinical use of the CTI when adding it into the baseline model used to predict the prognosis of that population. Finally, subgroup analysis was conducted to evaluate the interaction between the traditional cardiovascular risk factor and CTI-related cardiovascular outcomes. The calculation method of CTI was as followed: ln[triglyceride(mg/dl) × fasting blood glucose(mg/dl)/2] + 0.412 × ln (C-reactive protein). Results Among the 2797 PCI-treated patients with heart failure, 131 experienced MACCEs. Restricted cubic spline model showed that the CTI was significantly associated with the risk of adverse cardiovascular outcomes within 12 months (P for nonlinearity < 0.001), with a best cut-off value of 9.47. After adjusting for various confounders, the CTI remained independently associated with the incidence of endpoints (hazard ratio 1.41; 95%CI 1.13–1.77; P < 0.01) while the TyG index was not. Furthermore, Kaplan-Meier analysis demonstrated a higher incidence of endpoints (hazard ratio 1.55; 95%CI 1.11–2.16; Log rank P = 0.011) and all-cause death (hazard ratio 2.16; 95%CI 1.16–3.99; Log rank P = 0.015) in enrolled patients with high CTI (CTI ≥ 9.47). Adding the CTI into the baseline model used to predict the adverse outcomes improved the predictive ability for the endpoints (increase in C-statistic value from 0.685 to 0.694; NRI 0.217, 95% confidence interval 0.050–0.385, P = 0.011; IDI 0.003, 95% confidence interval 0.001–0.007, P = 0.049). Subgroup analysis showed that there existed an interaction between CTI and hypertension for the prediction of endpoints (P for interaction = 0.046). Conclusions Elevated CTI is associated with an increased risk of adverse cardiovascular outcomes in heart failure patients undergoing PCI, indicating the potential use of the CTI in the risk stratification and prognosis prediction of that population.

A 26-year-old woman with congenital heart disease, postatrial septal defect repair, postarterial catheter ligation, hypoxia-associated pulmonary hypertension, and reduced right heart function, which manifested as a severe decrease in activity tolerance, chest tightness and shortness of breath, and easy fatigue of breathing, was treated with oxygen, targeting medications such as anisentan, tadalafil, remodulin, and diuretic potassium supplementation to enhance cardiac function, and then her symptoms were slightly improved compared with the previous ones. She was guided with in-hospital respiratory training to the extent that the patient could tolerate it and then was discharged from the hospital to have a home-based respiratory rehabilitation for a period of 3 months. The training plan was as follows: (i) Respiratory muscle function test: the patient's resting maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) were assessed by the respiratory trainer equipment, and the respiratory muscle weakness/invulnerability was defined as a measured maximal pressure value less than 80 cmH2O according to the ERS guidelines.1 (ii) Respiratory muscle training impedance progression: first month, 30% of the MIP and MEP of this test, 30 repetitions/day, 5–7 days/week for 1 month; second month, reassessment of respiratory muscle strength with impedance of 35% of the MIP and MEP of this test, 30 repetitions/day, 5–7 days/week for 1 month; and month 3, reassessment of respiratory muscle strength with impedance of MIP and 40% of MEP, 30 times/day, 5–7 days/week for 1 month. During the period of home respiratory rehabilitation, this patient did not experience any adverse hazardous events. (1) After 3 months of training, this patient's respiratory muscle strength improved, including a significant increase in MIP from 43 to 53 cmH2O and a slight increase in MEP from 53 to 57 cmH2O; peak inspiratory flow rate decreased from 2.77 to 3.50 L/s, and peak expiratory flow rate decreased from 3.01 to 2.57 L/s. (2) This patient's oxygen saturation improved with oxygen (91% vs. 94%) and her heart rate decreased significantly without oxygen (102 vs. 90 bpm) compared to before training (91% vs. 94%). Additionally, her heart rate was significantly lower (102 vs. 90 bpm), and oxygen saturation was significantly better (83% vs. 89%) without oxygen than it was 3 months prior. (3) Subjective symptoms improved, with the patient initially completing a training session with a Borg score of up to 12/20. After training, she completed the same session with a Borg score of 9–10/20. (4) Weakness improved. Before training, the patient experienced more than moderate shortness of breath with minimal activity and needed a wheelchair while in an oxygenated state. After the training, she could go up and down three staircases or walk on the flat ground for 3–4 min with much less perceived dyspnea. Respiratory muscle weakness is common in patients with pulmonary arterial hypertension;2 patients with respiratory muscle weakness are prone to increased respiratory muscle work, which causes respiratory muscle fatigue, alters respiratory responses, and ultimately leads to exercise intolerance. Respiratory muscle training can increase inspiratory muscle strength and endurance. The abnormal performance associated with respiratory muscle weakness can be partially counteracted, thus improving exercise capacity. In addition to exercise rehabilitation in the conventional sense, more rehabilitation modalities have been shown to improve exercise tolerance in patients with cardiovascular disease, and respiratory muscle rehabilitation can be an important modality for home rehabilitation due to its simplicity and ease of implementation.3 We have seen significantly improved respiratory muscle strength, functional capacity, as well as dyspnea and fatigue in this complex pulmonary arterial hypertension patient after 3 months of respiratory muscle rehabilitation training, which is consistent with the findings of Saglam M et al.4 In addition to this, this patient had increased peripheral oxygen saturation and decreased heart rate after training compared to pretraining. Although both MIP and MEP improved in this patient, the respiratory muscle strength was still lower than the normal expected value, which indicated that the patient still had residual inspiratory muscle weakness, which may be related to the fact that sarcopenia is common in patients with pulmonary arterial hypertension, where respiratory muscle damage can be more severe than skeletal muscle damage, making it more difficult to improve the respiratory muscle strength.4-7 Also, the increased oxygen saturation and decreased heart rate in patients may be related to the fact that respiratory muscle training improves the efficiency of the patient's respiratory muscle6 and results in a decrease in the cardiac output required to do the work of breathing to maintain ventilation under the same conditions and some improvement in oxygen kinetics.4, 8, 9 It has also been shown that increasing inspiratory muscle strength increases the ventilatory load required for the onset of metabolic reflexes,10, 11 which can increase peripheral muscle blood flow and oxygenation during exercise in patients with heart failure,10 thus potentially delaying the onset of fatigue, which may also contribute to the improvement in exercise capacity and subjective symptoms in this patient. Although the guidelines suggest cardiac rehabilitation in patients with pulmonary arterial hypertension, including a variety of rehabilitation modalities, it is not possible to carry out a wide range of rehabilitation therapies in the clinical reality of dealing with critically ill patients. Therefore, it is particularly important to choose the appropriate rehabilitation introduction technique to provide a starting point for a more comprehensive rehabilitation treatment and to suggest confidence in the patient's recovery. We are in the process of relevant research to clarify exactly which rehabilitation treatment can be used as this initial rehabilitation treatment. This patient's results are in line with our research expectations, and respiratory muscle rehabilitation may be an option as an introduction therapy. Low oxygen saturation is an important cause of patients' quality of life, which is also an important indicator of the impact of disease risk stratification. This type of respiratory muscle rehabilitation, which can be implemented under home conditions, can help patients to improve their oxygen saturation even when their respiratory muscle strength is not elevated, with the aim of improving their quality of life and reducing the risk stratification of the disease. Xinxin Yan and Ya Song reviewed the literature and wrote the manuscript; Xinxin Yan and Ya Song supervised and revised the manuscript. All authors read and approved the final manuscript. This study was financially supported from The Basic Research Program for Beijing–Tianjin–Hebei Coordination under grant no. 19JCZDJC65500(Z), Chinese Academy of Medical Science Health Innovation Project (grant nos. 2021-I2M-1-042, 2021-I2M-1-058, and 2022-I2M-C&T-A-005), Tianjin Outstanding Youth Fund Project (grant no. 20JCJQIC00230), and CAMS Innovation Fund for Medical Sciences (CIFMS) (grant no. 2022-I2M-C&T-B-012). The authors declare no conflict of interest. Approved by the Institutional Review Board and Ethics Committee of FuWai Hospital (Approval No. 2022-1686, Approval Date: 2022-3-8), and informed consent have been properly documented.

BACKGROUND:The incidence of arterial stenosis is increasing year by year. In order to better diagnose and treat arterial stenosis, numerical simulation technology has become a popular method.OBJECTIVE:A novel model is constructed to investigate the influence of microcirculation on the hemodynamics of artery bypass graft.METHODS:In this paper, a severely narrow artery bypass graft model is considered. The geometric shape includes a narrow artery tube and a bypass graft of the same diameter with a 45° suture angle. The fluid-structure interaction model is considered by finite element numerical calculation, and the flow is simulated with microcirculation as the outlet boundary condition. The changes of blood flow velocity, pressure and wall shear stress are analyzed.RESULTS:The results show that blood almost entirely flows into the graft tube and there is no recirculation area at the anastomosis.CONCLUSION:The artery bypass graft model considering microcirculation function could simulate the physiological characteristics of blood flow more reasonably, and it provide helps for clinicians to diagnose and treat arterial stenosis.