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Both aging and high blood pressure (BP) are associated with a risk of left ventricular concentricity and hypertrophy. We hypothesized that optimal BP management improves left ventricular remodeling beyond aging. Among 558 hypertensive patients on continuous antihypertensive treatment and without concurrent heart disease who were referred to a cardiology clinic with echocardiography and ambulatory BP monitoring data, 142 patients' echocardiographic data was available after 10 years. Baseline BP and changes in left ventricular geometry were evaluated. Mean age at baseline was 71.0 years old. Baseline daytime BP was 129.9/72.4 ± 17.1/10.2 mmHg and nighttime BP was 122.5/67.1 ± 16.9/9.1 mmHg. After 10 years, left ventricular mass index (LVMI) and relative wall thickness (RWT) significantly decreased from 104.5 ± 26.3 to 97.9 ± 26.4 g/m2, p = 0.003 and 0.51 ± 0.09 to 0.47 ± 0.09, p < 0.001, consecutively. Among patients with hypertrophic geometry at baseline, 17.2% reverted to normal geometry at follow-up. Daytime systolic BP (136.9 ± 18.5 mmHg vs 126.2 ± 16.5 mmHg, p = 0.03), nighttime systolic BP (126.2 ± 17.7 mmHg vs 116.3 ± 16.0 mmHg, p = 0.038) and daytime pulse pressure (63.5 ± 17.3 mmHg vs 53.1 ± 14.9 mmHg, p = 0.022) at baseline were higher in patients who remained hypertrophic than those without hypertrophy at follow-up. On logistic regression analysis, daytime, nighttime systolic BP, and daytime pulse pressure were significantly related to the regression of hypertrophy adjusted for age, sex, eGFR, BMI, LVMI, and RWT at baseline. For conclusion, antihypertensive treatment for 10 years improved LV geometry despite aging. Ambulatory BP and pulse pressure at baseline predicted the change of LV geometry after 10 years.

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Aortic regurgitation (AR) is associated with left ventricular volume and pressure overload, resulting in eccentric left ventricular (LV) remodeling and enlargement. This condition may be well tolerated for years before the onset of myocardial dysfunction and symptoms. Echocardiography plays a crucial role in the diagnosis of AR, assessing its mechanism and severity, and detecting LV remodeling. The assessment of AR severity is challenging and frequently requires the integration of information from multiple different measurements to assess the severity. Recent data suggests that echocardiographically derived LV volumes (end-systolic volume index > 45 ml/m2), an ejection fraction threshold of <60%, and abnormal global longitudinal strain may help identify early dysfunction and may be used to improve clinical outcomes. Consequently, these parameters can identify candidates for surgery. Cardiac magnetic resonance imaging is emerging as a valuable tool for assessing severity when it remains unclear after an echocardiographic evaluation. This review emphasizes the importance of imaging, particularly echocardiography, in the evaluation of AR. It focuses on various echocardiographic parameters, including technical details, and how to integrate them for assessing the mechanism and severity of AR, as well as LV remodeling.

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The erythrocyte S1P transporter Mfsd2b is also expressed in the heart. We hypothesized that S1P transport by Mfsd2b is involved in cardiac function. Hypertension-induced cardiac remodeling was induced by 4-weeks Angiotensin II (AngII) administration and assessed by echocardiography. Ca2+ transients and sarcomere shortening were examined in adult cardiomyocytes (ACM) from Mfsd2b+/+ and Mfsd2b-/- mice. Tension and force development were measured in skinned cardiac fibers. Myocardial gene expression was determined by real-time PCR, Protein Phosphatase 2A (PP2A) by enzymatic assay, and S1P by LC/MS, respectively. Msfd2b was expressed in the murine and human heart, and its deficiency led to higher cardiac S1P. Mfsd2b-/- mice had regular basal cardiac function but were protected against AngII-induced deterioration of left-ventricular function as evidenced by ~ 30% better stroke volume and cardiac index, and preserved ejection fraction despite similar increases in blood pressure. Mfsd2b-/- ACM exhibited attenuated Ca2+ mobilization in response to isoprenaline whereas contractility was unchanged. Mfsd2b-/- ACM showed no changes in proteins responsible for Ca2+ homeostasis, and skinned cardiac fibers exhibited reduced passive tension generation with preserved contractility. Verapamil abolished the differences in Ca2+ mobilization between Mfsd2b+/+ and Mfsd2b-/- ACM suggesting that S1P inhibits L-type-Ca2+ channels (LTCC). In agreement, intracellular S1P activated the inhibitory LTCC phosphatase PP2A in ACM and PP2A activity was increased in Mfsd2b-/- hearts. We suggest that myocardial S1P protects from hypertension-induced left-ventricular remodeling by inhibiting LTCC through PP2A activation. Pharmacologic inhibition of Mfsd2b may thus offer a novel approach to heart failure.

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Objectives: The aim of this meta-analysis is to evaluate the effect of astragalus injection (AI) on left ventricular remodeling (LVR) in patients with heart failure with mildly reduced ejection fraction (HFmrEF). Methods: The randomized controlled trials (RCTs) of AI in treating HFmrEF were retrieved from 8 major English and Chinese electronic databases, up until November 30, 2023. To evaluate the methodological quality of the included studies, the Cochrane bias risk tool and the Modified Jadad Scale were employed. Stata 17.0 software was utilized for statistical analysis, sensitivity analysis, and assessment of publication bias. Results: Ten RCTs with 995 patients (562 males and 433 females) were identified. Meta-analysis indicated that compared to conventional treatment (CT), AI significantly improved LVR, specifically increasing left ventricular ejection fraction (LVEF, MD = 4.56, 95% CI: 3.68-5.44, p < 0.00001), decreasing left ventricular end-diastolic volume (LVEDV, MD = -7.89, 95% CI: -11.13 to -4.64, p < 0.00001), left ventricular end-diastolic diameter (LVEDD, MD = -4.18, 95% CI: -5.79 to -2.56, p < 0.00001), left ventricular end-systolic volume (LVESV, MD = -8.11, 95% CI: -11.79 to -4.43, p < 0.00001), and left ventricular end-systolic diameter (LVESD, MD = -3.42, 95% CI: -4.90 to -1.93, p < 0.00001). AI also improved clinical efficacy (RR = 4.62, 95% CI: 3.11-6.88, p < 0.00001), reduced N-terminal pro-brain natriuretic peptide (NT-pro BNP, MD = -27.94, 95% CI: -43.3 to -12.36) level, without increasing the incidence of adverse reactions (RR = 1.60, 95% CI: 0.59-4.29, p = 0.35). Sensitivity analysis confirmed the reliability of the merged results, and Begg's and Egger's tests showed no significant publication bias. Conclusion: The systematic review and meta-analysis revealed that combining AI with CT improves LVR without increasing adverse events in HFmrEF patients. However, caution is needed in interpreting the results due to limited evidence. Future high-quality RCTs are needed to support these conclusions. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, PROSPERO [CRD42022347248].

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BACKGROUND: Despite improved treatments for acute myocardial infarction (AMI), myocardial fibrosis remains a key driver of adverse left ventricular (LV) remodeling and increased mortality. Fibroblast activation and proliferation significantly contribute to this process by enhancing cardiac fibrosis, which can lead to detrimental changes in LV structure. This study evaluates the effectiveness of 99mTc-labeled fibroblast activation protein inhibitor (99mTc-HFAPi) SPECT imaging in predicting LV remodeling over 12 months in post-AMI patients. METHODS: A cohort of 58 AMI patients (46 males, median age 61 [53, 67] years) underwent baseline 99mTc-HFAPi imaging (5 ± 2 days post-MI), perfusion imaging (6 ± 2 days post-MI), and echocardiography (2 ± 2 days post-MI). Additionally, 15 patients had follow-up 99mTc-HFAPi and perfusion imaging, while 30 patients had follow-up echocardiography. Myocardial 99mTc-HFAPi activity was assessed at the patient level. LV remodeling was defined as a ≥10% increase in LV end-diastolic diameter (LVEDD) or LV end-systolic diameter (LVESD) from baseline to follow-up echocardiography. RESULTS: AMI patients displayed localized but non-uniform 99mTc-HFAPi uptake, exceeding perfusion defects. Baseline 99mTc-HFAPi activity exhibited significant correlations with BNPmax, LDHmax, cTNImax, and WBCmax, inversely correlating with LVEF. After 12 months, 11 patients (36.66%) experienced LV remodeling. Univariate regression analysis demonstrated an association between baseline 99mTc-HFAPi uptake extent and LV remodeling (OR = 2.14, 95%CI, 1.04, 4.39, P = 0.038). CONCLUSIONS: 99mTc-HFAPi SPECT imaging holds promise in predicting LV remodeling post-MI, providing valuable insights for patient management and prognosis.

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OBJECTIVE: Bicuspid aortic valve (BAV) is prone to promote left ventricular remodeling (LVR), which is associated with adverse clinical outcomes. Although the association between angiogenic activity and LVR has been established, pro-angiogenic cytokine features and potential biomarker candidates for LVR in patients with BAV remain to be clarified. METHODS: From November 2018 to May 2019, patients with BAV diagnosed by transthoracic echocardiography at our institution were included. LVR was diagnosed on the basis of echocardiographic calculations of relative wall thickness (RWT) and left ventricular mass index (LVMI). A multiplex ELISA array was used to measure the plasma levels of 60 angiogenesis-related cytokines. RESULTS: Among 103 patients with BAV, 71 were categorized into the LVR group and 32 into the normal left ventricular (LV) geometry group. BAV patients with LVR demonstrated increased LVMI, elevated prevalence of moderate to severe aortic stenosis and aortic regurgitation, and decreased LV ejection fraction (LVEF). Plasma levels of angiopoietin-1 were elevated in BAV patients with or without LVR compared with healthy controls (P = 0.001, P < 0.001, respectively), and were negatively correlated with RWT (r = -0.222, P = 0.027). Plasma levels of angiopoietin-2 were elevated in the LVR group (P = 0.001) compared with the normal LV geometry group, and were negatively correlated with LVEF (r = -0.330, P = 0.002). CONCLUSION: Decreased angiogenesis plays a crucial role in the occurrence and progression of LVR in patients with BAV. Disturbance in the pro- and anti-angiogenesis equilibrium in BAV patients with LVR may reflect the aggravation of endothelial injury and dysfunction.

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Cardiac fibrosis can be mitigated by limiting fibroblast-to-myofibroblast differentiation and proliferation. Human antigen R (HuR) modulates messenger RNA stability and expression of multiple genes. However, the direct role of cardiac myofibroblast HuR is unknown. Myofibroblast-specific deletion of HuR limited cardiac fibrosis and preserved cardiac functions in pressure overload injury. Knockdown of HuR in transforming growth factor-ß1-treated cardiac fibroblasts suppressed myofibroblast differentiation and proliferation. HuR deletion abrogated the expression and messenger RNA stability of cyclins D1 and A2, suggesting a potential mechanism by which HuR promotes myofibroblast proliferation. Overall, these data suggest that inhibition of HuR could be a potential therapeutic approach to limit cardiac fibrosis.

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OBJECTIVE: To evaluate the predictive value of global longitudinal strain (GLS) measured by cardiac magnetic resonance (CMR) feature-tracking technique for left ventricular remodeling (LVR) after percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI). METHODS: A total of 403 patients undergoing PCI for acute STEMI were prospectively recruited from multiple centers in China.CMR examinations were performed one week (7±2 days) and 6 months after myocardial infarction to obtain GLS, global radial strain (GRS), global circumferential strain (GCS), ejection fraction (LVEF) and infarct size (IS).The primary endpoint was LVR, defined as an increase of left ventricle end-diastolic volume by ≥20% or an increase of left ventricle end-systolic volume by ≥15% from the baseline determined by CMR at 6 months.Logistic regression analysis was performed to evaluate the predictive value of CMR parameters for LVR. RESULTS: LVR occurred in 101 of the patients at 6 months after myocardial infarction.Compared with those without LVR (n=302), the patients in LVR group exhibited significantly higher GLS and GCS (P < 0.001) and lower GRS and LVEF (P < 0.001).Logistic regression analysis indicated that both GLS (OR=1.387, 95%CI: 1.223-1.573;P < 0.001) and LVEF (OR=0.951, 95%CI: 0.914-0.990;P=0.015) were independent predictors of LVR.ROC curve analysis showed that at the optimal cutoff value of-10.6%, GLS had a sensitivity of 74.3% and a specificity of 71.9% for predicting LVR.The AUC of GLS was similar to that of LVEF for predicting LVR (P=0.146), but was significantly greater than those of other parameters such as GCS, GRS and IS (P < 0.05);the AUC of LVEF did not differ significantly from those of the other parameters (P>0.05). CONCLUSION: In patients receiving PCI for STEMI, GLS measured by CMR is a significant predictor of LVR occurrence with better performance than GRS, GCS, IS and LVEF.

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BACKGROUND: Cardiac magnetic resonance (cMRI) is often used to diagnose acute myocarditis (AM). It is also performed after 6 months to monitor myocardial involvement. However, the clinical and predictive relevance of the 6-month cMRI is uncertain. OBJECTIVE: We used cMRI to assess the morphology and heart function of patients with AM, the correlation between left ventricular remodeling and biomarkers of heart dysfunction and myocardial fibrosis, and the involvement of myocardial fibrosis initially and 6 months after the acute episode. MATERIALS AND METHODS: We conducted a prospective study of 90 patients with the clinical suspicion of AM, where cMRI was performed within the first week after symptom onset and repeated after 6 months. RESULTS: Non-ischemic late gadolinium enhancement (LGE) was present in 88 (97.7%) patients and mainly involved the septum and inferior wall. cMRI at 6 months was associated with significantly reduced abnormalities of segmental kinetics (p < 0.001), myocardial edema (p < 0.001), presence of LGE (p < 0.05) and LGE mass (p < 0.01), native T1 mapping (p < 0.001), and presence of pericardial collection (p ≤ 0.001). At 6 months, signs of myocardial edema appeared in 34.4% of patients, and a complete cure (absence of edema and LGE) was found in 8.8% of patients. LGE disappeared in 15.2% of patients, and the mean number of myocardial segments involved decreased from 46% to 30%, remaining unchanged in 13% of patients. Patients with LGE without edema had a more severe prognostic condition than those with persistent edema. Patients with increased LGE extension on the control cMRI had a worse prognosis than those with modified or low LGE. The most significant independent predictive parameters for major cardiovascular events (MACEs) were LGE mass (adjusted OR = 1.27 [1.11-1.99], p < 0.001), myocardial edema (OR = 1.70 [1.14-209.3], p < 0.001), and prolonged native T1 (OR = 0.97 [0.88-3.06], p < 0.001). The mid-wall model of LGE and the presence of edema-free LGE were MACE-independent predictors. CONCLUSIONS: LGE, myocardial edema, and prolonged native T1 were predictors of MACEs. LGE does not necessarily mean constituted fibrosis in the presence of edema and may disappear over time. LGE without edema could represent fibrosis, whereas the persistence of edema represents active inflammation and could be associated with the residual chance of complete recovery. cMRI should be performed in all patients with AM at 6 months to evaluate progress and prognosis.

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Background: Secreted frizzled-related protein 2 (sFRP2) is involved in various cardiovascular diseases. However, its relevance in left ventricular (LV) remodeling in patients with hypertension (HTN) is obscure. Methods: In this study, 196 patients with HTN were included, 59 with echocardiographic LV remodeling. A total of 100 healthy subjects served as normal controls. The serum-sFRP2 level was measured by enzyme-linked immunosorbent assay (ELISA). Data were collected from medical records for baseline characteristics, biochemistry tests, and echocardiography. Receiver operating characteristic (ROC) curves were used to assess the distinguishing value of sFRP2 for LV remodeling in patients with HTN. Spearman rank correlation analysis was utilized to identify factors correlated with sFRP2. Cardiac sFRP2 was determined by Western blot and quantitative polymerase chain reaction (qPCR). Results: The level of serum-sFRP2 was higher in HTN patients with echocardiographic LV remodeling than their non-remodeling counterparts. ROC analysis showed that the area under the curve (AUC) for sFRP2 in distinguishing echocardiographic LV remodeling in HTN patients was 0.791 (95% confidence interval (CI): 0.714-0.869). The sFRP2 was negatively correlated with LV dimension and positively correlated with relative wall thickness (RWT). The expression of sFRP2 was higher in hypertrophic hearts, which could be reversed by myricetin. Conclusions: The serum level and cardiac sFRP2 increased in the setting of LV remodeling and decreased by myricetin. Serum sFRP2 may be a promising distinguishing factor for LV remodeling in HTN patients.

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BACKGROUND: Despite the close association between aortic stenosis (AS) and cardiac damage (CD), it is unclear if CD is limited to patients with moderate and severe AS and which factors affect its progression. Although altered valvular hemodynamic status may drive the development of CD in AS, commonly occurring comorbidities may contribute. OBJECTIVES: The aim of this study was to determine the prevalence of and factors associated with CD in mild AS. METHODS: This retrospective study included 9,611 patients with mild AS (peak aortic valve velocity [Vmax] 2-3 m/s and description of abnormal aortic valve) from 2010 through 2021. CD was staged using the Genereux classification. RESULTS: All but 20% (n = 1,901; stage 0) of patients with mild AS demonstrated CD: 1,613 (17%) stage 1, 4,843 (50%) stage 2, 891 (9%) stage 3, and 363 (4%) stage 4. Patients with higher stages had more comorbidities (hypertension, heart failure, ischemic heart disease, stroke, peripheral arterial disease, chronic kidney disease, chronic pulmonary disease, and diabetes mellitus) but had valvular hemodynamic status similar to those without CD. CD stage did not worsen with higher Vmax range (stage >1 in 64% with Vmax <2.5 m/s vs 61% with Vmax ≥2.5 m/s) but increased with the number of comorbidities, with stage >1 occurring in 50%, 53%, 60%, 66%, 72%, and 73% in the presence of 0, 1, 2, 3, 4, and 5 or more comorbidities, respectively. CONCLUSIONS: CD was highly prevalent in patients with mild AS. Among patients with mild AS, there was no relationship between the degree of CD and AS severity; instead, CD was highly associated with comorbidities.

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OBJECTIVE: To investigate the effects of different blood purification modes on left ventricular remodeling and its relationship with serum cardiac troponin I (cTnI) in patients with end-stage renal disease (ESRD). METHOD: A total of 108 patients with ESRD were selected, 55 cases were divided into hemodialysis combined with hemoperfusion (HD + HP) group, in which patients participants accepted routine hemodialysis for three times/week and hemoperfusion for three times/month; 53 cases in hemodialysis combined with hemodialysis filtration (HD + HDF) group, routine hemodialysis three times/week + hemodialysis filtration three times/month. The total duration of dialysis in the study was 1 year. Cardiac troponin I (cTnI) levels were measured before dialysis and 1 year after treatment, and related parameters were measured by echocardiography, including ventricular septal thickness (IVST), left ventricular posterior wall thickness (LVPWT), left ventricular end diastolic diameter (LVEDd), left ventricular end systolic diameter (LVEDs), and left ventricular myocardial mass index (LVMI). The paired t test was used within the group. Correlation analysis was performed using Spearman correlation analysis. RESULT: After treatment, the levels of cTnI, IVST, LVPWT, LVEDd, LVEDs, and LVMI in the two groups were increased, and the results were statistically significant (all p < 0.05). In addition, cTnI of the two groups was significantly correlated with IVST, LVPWT, LVEDd, LVEDs, and LVMI (all p < 0.05). CONCLUSION: Left ventricular remodeling is common in patients with ESRD, HD + Hp, and HD + HDF cannot reduce the phenomenon of left ventricular remodeling, cTnI can be used as a predictor of left ventricular hypertrophy and enlargement.

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Low-flow (LF) aortic stenosis (AS) is common among older adults and associated with worse outcomes than AS with normal stroke volume. It is unknown whether left ventricular (LV) remodeling identifies patients with LF AS at higher risk of complications. LV remodeling was evaluated in 463 patients with severe LF AS referred for transcatheter aortic valve replacement (TAVR) and classified as adaptive (normal geometry and concentric remodeling) or maladaptive (concentric and eccentric hypertrophy) using the American Society of Echocardiography gender-specific criteria. Of these, the 390 patients who underwent TAVR were followed for the end points of heart failure (HF) hospitalization and all-cause mortality. The mean patient age was 79 (74.5 to 84) years. LV remodeling was adaptive in 57.4% (62 normal geometry, 162 concentric remodeling) and maladaptive in 42.6% (127 concentric hypertrophy, 39 eccentric hypertrophy). During a median follow-up of 3 years, 45 patients (11.5%) were hospitalized for HF and 73 (18.7%) died. After adjustment for widely used echocardiographic parameters, maladaptive remodeling was independently associated with HF hospitalization and death (adjusted hazard ratio 1.75, confidence interval 1.03 to 3.00). There was no significant difference between men and women in the association of maladaptive LV remodeling with the composite outcome (p = 0.40 for men and p = 0.06 for women). In conclusion, in patients with LF AS, maladaptive LV remodeling before TAVR is independently associated with higher incidences of postprocedural HF rehospitalization and death in both men and women. Assessment of LV remodeling has prognostic value over and above LV ejection fraction and may improve risk stratification for patients with LF AS.

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OBJECTIVE: To analyze the effect of sacubitril-valsartan on left ventricular remodeling and NT-proBNP in heart failure patients with hypertension and reduced ejection fraction. METHOD: A retrospective analysis was conducted on 112 heart failure patients with reduced ejection fraction (HFrEF) and concomitant hypertension who were treated in Baoji Central Hospital from May 2019 to October 2021. Standard heart failure treatment was applied in both groups. Besides, the observation group (n=60) was additionally treated with sacubitril/valsartan (initial dose of 50 mg twice daily, adjusted every 2-4 weeks by doubling the dose to a maximum of 200 mg twice daily based on the patients' actual conditions and tolerance), and the control group (n=52) received valsartan (80 mg once daily). The treatment duration for both groups was 6 months. Therapeutic efficacy, blood pressure, echocardiographic parameters, N-terminal pro-brain natriuretic peptide (NT-proBNP) and left ventricular remodeling before and after treatment were recorded and compared between the two groups, as well as the adverse drug reactions during the treatment and life quality after treatment. Finally, multifactor regression analysis was performed to screen the independent risk factors affecting patient prognosis. RESULTS: Compared with the CG, the overall response rate in the OG was evidently higher (P < 0.001); the improvements in blood pressure, NT-proBNP, interventricular septal thickness (IVST), left ventricular posterior wall thickness (LVPWT) and left ventricular mass index (LVMI) were more significant in the OG (all P < 0.001). Both groups showed marked improvements in left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD) and (left ventricular end-systolic diameter) LVESD compared to baseline, with more significant improvement in the OG compared with the CG (all P < 0.001). There was no significant difference in the incidence of adverse reactions between the two groups. However, post-treatment quality of life was much higher in the OG compared to the CG (P < 0.001). Comorbid diabetes and treatment regimen were identified as independent risk factors affecting patient prognosis. CONCLUSION: Sacubitril-valsartan can effectively improve blood pressure, cardiac function and ventricular remodeling in patients with HFrEF and hypertension without increasing adverse reactions. It is highly safe and worthy of clinical promotion.

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Background: Sacubitril-valsartan has been widely reported for reducing the risk of cardiovascular death and improving left ventricular remodeling in patients with heart failure (HF). However, the effect of sacubitril-valsartan in patients with acute myocardial infarction (AMI) remains controversial. Therefore, we conducted this meta-analysis to investigate whether sacubitril-valsartan could reverse left ventricular remodeling and reduce cardiovascular adverse events in AMI patients after primary percutaneous coronary intervention (PPCI). Materials and methods: Two researchers independently retrieved the relevant literature from PubMed, Embase, The Cochrane Library, China National Knowledge Infrastructure (CNKI), and the Wanfang database. The retrieval time was limited from inception to 1 June 2023. Randomized controlled trials (RCTs) meeting the inclusion criteria were included and analyzed. Results: In total, 21 RCTs involving 2442 AMI patients who underwent PPCI for revascularization were included in this meta-analysis. The meta-analysis showed that compared with the angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB), sacubitril-valsartan treatment in AMI patients after PPCI significantly reduced left ventricular end-diastolic dimension (LVEDD) (weighted mean difference (WMD) -3.11, 95%CI: -4.05∼-2.16, p < 0.001), left ventricular end-diastolic volume (LVEDV) (WMD -7.76, 95%CI: -12.24∼-3.27, p = 0.001), left ventricular end-systolic volume (LVESV) (WMD -6.80, 95%CI: -9.45∼-4.15, p < 0.001) and left ventricular end-systolic dimension (LVESD) (WMD -2.53, 95%CI: -5.30-0.24, p < 0.001). Subgroup analysis according to the dose of sacubitril-valsartan yielded a similar result. Meanwhile, PPCI patients using sacubitril-valsartan therapy showed lower risk of major adverse cardiac events (MACE) (OR = 0.36, 95%CI: 0.28-0.46, p < 0.001), myocardial reinfarction (OR = 0.54, 95%CI: 0.30-0.98, p = 0.041) and HF (OR = 0.35, 95%CI: 0.26-0.47, p < 0.001) without increasing the risk of renal insufficiency, hyperkalemia, or symptomatic hypotension. At the same time, the change of LV ejection fraction (LVEF) (WMD 3.91, 95%CI: 3.41-4.41, p < 0.001), 6 min walk test (6MWT) (WMD 43.56, 95%CI: 29.37-57.76, p < 0.001) and NT-proBNP level (WMD -130.27, 95%CI: -159.14∼-101.40, p < 0.001) were statistically significant. Conclusion: In conclusion, our meta-analysis indicates that compared with ACEI/ARB, sacubitril-valsartan may be superior to reverse left ventricular remodeling, improve cardiac function, and effectively reduce the risk of MACE, myocardial reinfarction, and HF in AMI patients after PPCI during follow-up without increasing the risk of adverse reactions including renal insufficiency, hyperkalemia, and symptomatic hypotension.

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PURPOSE: We sought to detect left ventricular (LV) adverse alterations in structure and function in type 2 diabetes mellitus (T2DM) patients with or without mild renal dysfunction (MRD) using comprehensive echocardiography techniques and to explore the independent risk factors for LV remodeling (LVR) and dysfunction in these patients. METHODS: The study included 82 T2DM patients with normal LV ejection fraction (presence (n = 42)/absence (n = 40) of MRD). Age- and gender-matched controls (n = 40) were also recruited. LV structure and function were evaluated using conventional echocardiography and three-dimensional speckle tracking echocardiography (3DSTE). Global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS) were all measured using 3DSTE. RESULTS: Compared with the controls with absolute advantage of LV normal geometry, LVR was more frequently present in the two T2DM groups, with the largest proportion in those with T2DM and MRD (P < 0.001). Fasting plasma glucose (FPG) and MRD were both significant risk factors for LVR in T2DM patients. The detection rates of LV diastolic dysfunction and subclinical systolic dysfunction were significantly higher in the T2DM groups than in the controls (P = 0.000). Moreover, the two case groups also showed significantly lower strain values in multiple directions than the controls (all P < 0.05). FPG was significantly associated with LV diastolic dysfunction, whereas FPG and MRD were both significantly associated with subclinical LV systolic dysfunction in T2DM patients. CONCLUSIONS: The combined use of conventional echocardiography and 3DSTE allowed the timely detection of early cardiac damage in T2DM patients with or without MRD.

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Background: Chronic heart failure (CHF) is a prevalent and highly challenging cardiovascular disease associated with high mortality rates. The occurrence and progression of CHF are closely linked to left ventricular remodeling (LVR) and inflammation. Addressing LVR and reducing inflammation can significantly slow down the progression of CHF and improve patient prognosis. Objective: To evaluate the effects of Xinmailong injection (XMLI) on LVR and inflammatory mediators in CHF patients. Method: The randomized controlled trials investigating the effectiveness of XMLI treatment for CHF were retrieved from eight databases up until 31 December 2023. To evaluate the methodological quality of included studies, the Cochrane bias risk tool was employed. Furthermore, statistical analysis, sensitivity analysis, and publication bias assessment were conducted using Stata 17.0 software. Result: Compared with conventional treatment (CT), the combination therapy of XMLI and CT significantly improved LVR and reduced inflammatory mediators, mainly manifested by an increase in LVEF (MD = 6.40, 95% CI: 5.25 to 7.55, p = 0.000), a decrease in LVEDD (MD = -4.63, 95% CI: -5.69 to -3.57, p = 0.000) and LVESD (MD = -4.00, 95% CI: -5.50 to -2.50, p = 0.000), as well as a decrease in TNF-α (MD = -7.93, 95% CI: -9.86 to -6.00, p = 0.000), IL-6 (MD = -5.25, 95% CI: -6.59 to -3.92, p = 0.000), IL-18 (MD = -36.07, 95% CI: -46.76 to -25.38, p = 0.000), CRP (MD = -4.41, 95% CI: -6.40 to -2.42, p = 0.000), hs-CRP (MD = -4.90, 95% CI: -5.71 to -4.08, p = 0.000), and an increase in IL-10 (MD = 20.19, 95% CI: 10.42 to 29.97, p = 0.000). In addition, the combination therapy showed enhanced clinical efficacy (OR = 4.08, 95% CI: 3.10 to 5.37, p = 0.000), decreased expression levels of BNP (MD = -138.48, 95% CI: -155.48 to -121.48, p = 0.000), and NT-pro BNP (MD = -315.63, 95% CI: -359.25 to -272.00, p = 0.000), and increased the 6-MWD (MD = 71.02, 95% CI: 57.23 to 84.81, p = 0.000). It is noteworthy that the combination therapy did not lead to an increase in the incidence of adverse reactions (OR = 1.01, 95% CI: 0.68 to 1.50, p = 0.97). Conclusion: This systematic review and meta-analysis demonstrated the superiority of combining XMLI and CT therapies over CT alone in improving LVR and reducing inflammatory mediators in patients with CHF. Importantly, this combination therapy does not increase adverse reactions. However, it is crucial to exercise caution while interpreting the survey results due to the limited quality of the included studies.Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=492715, Identifier CRD42023492715.

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OBJECTIVE: To assess the value of cardiac magnetic resonance (CMR) imaging for predicting adverse left ventricular remodeling in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: We retrospectively analyzed the clinical data and serial CMR (cine and LGE sequences) images of 86 STEMI patients within 1 week and 5 months after percutaneous coronary intervention (PCI), including 25 patients with adverse LV remodeling and 61 without adverse LV remodeling, defined as an increase of left ventricular end-systolic volume (LVESV) over 15% at the second CMR compared to the initial CMR. The CMR images were analyzed for LV volume, infarct characteristics, and global and infarct zone myocardial function. The independent predictors of adverse LV remodeling following STEMI were analyzed using univariate and multivariate Logistic regression methods. RESULTS: The initial CMR showed no significant differences in LV volume or LV ejection fraction (LVEF) between the two groups, but the infarct mass and microvascular obstructive (MVO) mass were significantly greater in adverse LV remodeling group (P < 0.05). Myocardial injury and cardiac function of the patients recovered over time in both groups. At the second CMR, the patients with adverse LV remodeling showed a significantly lower LVEF, a larger left ventricular end-systolic volume index (LVESVI) and a greater extent of infarct mass (P < 0.001) with lower global peak strains and strain rates in the radial, circumferential, and longitudinal directions (P < 0.05), infarct zone peak strains in the 3 directions, and infarct zone peak radial and circumferential strain rates (P < 0.05). The independent predictors for adverse LV remodeling following STEMI included the extent of infarct mass (AUC=0.793, 95% CI: 0.693-0.873; cut-off value: 30.67%), radial diastolic peak strain rate (AUC=0.645, 95% CI: 0.534-0.745; cut-off value: 0.58%), and RAAS inhibitor (AUC= 0.699, 95% CI: 0.590-0.793). CONCLUSION: The extent of infarct mass, peak radial diastolic strain rate, and RAAS inhibitor are independent predictors of adverse LV remodeling following STEMI.

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Background: The triglyceride-glucose (TyG) index is a marker of insulin resistance and is associated with cardiovascular mortality and morbidity. Left ventricular remodeling (LVR) after myocardial infarction (STEMI) is associated with poor prognosis. Methods: This retrospective study included 293 STEMI patients. Echocardiography was performed before discharge and 3 months after MI. Results: Compared with the non-LVR group, TyG index value was found to be higher in the LVR group (p < 0.001). Logistic regression analysis showed that higher maximal troponin I value, higher calculated TyG index value, higher N-terminal prohormone of brain natriuretic peptide level and the presence of anterior MI were independently associated with the development of LVR. Conclusion: A high TyG index level may contribute to the prediction of LVR in nondiabetic STEMI patients undergoing successful primary percutaneous coronary intervention.

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