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Following an acute myocardial infarction (AMI), patients remain at risk for subsequent cardiovascular (CV) events. In the AEGIS-II trial, CSL112, a human apolipoprotein A-I derived from plasma that enhances cholesterol efflux, did not significantly reduce the first occurrence of CV death, myocardial infarction (MI), or stroke through 90 days compared with placebo. However, an analysis involving only the first event may not capture the totality of the clinical impact of an intervention because patients may experience multiple events. This prespecified exploratory analysis examines the effect of CSL112 on total burden of nonfatal ischemic events (ie, recurrent MI and stroke) and CV death. A total of 18,219 patients with AMI, multivessel coronary artery disease, and additional CV risk factors were randomized to either 4 weekly infusions of 6 g CSL112 (n = 9,112) or matching placebo (n = 9,107). A negative binomial regression model was applied to estimate the effect of CSL112 compared with placebo on the rate ratio (RR) of ischemic events. For CV death, MI, and stroke, there were numerically fewer total events at 90 days (503 vs 545 events; rate ratio [RR]: 0.88; 95% CI: 0.76-1.03, P = 0.11), and nominally significantly fewer total events at 180 days (745 vs 821 events, RR: 0.87; 95% CI: 0.77-0.99; P = 0.04) and 365 days (1,120 vs 1,211 events; RR: 0.89; 95% CI: 0.80-0.99; P = 0.04). Subsequent events constituted 13% of events at 90 days, 17% at 180 days, and 22% at 1 year. Similar findings were seen with the total occurrence of nonfatal MI and CV death. When type II MIs, unlikely to be modified by enhancing cholesterol efflux, were excluded, there were nominally significant reductions in the total occurrence of nonfatal MI (excluding type 2) and CV death at all time points (90 days: RR: 0.81; 95% CI: 0.68-0.97; P = 0.02; 180 days: RR: 0.82; 95% CI: 0.71-0.95; P < 0.01; 365 days: RR: 0.86; 95% CI: 0.76-0.98; P = 0.02). In this prespecified exploratory analysis of the AEGIS-II trial, 4 weekly infusions of CSL112 among high-risk patients after AMI significantly reduced the total burden of nonfatal ischemic events and CV death at 180 and 365 days compared with placebo. (AEGIS-II [Study to Investigate CSL112 in Subjects With Acute Coronary Syndrome]; NCT03473223) [ABSTRACT FROM AUTHOR]

Background: Myocardial Infarction still persists as the most prevalent cardiovascular disease and is a top cause of morbidity and mortality in doxorubicin treated cancer patients. This study evaluated the prophylactic effect of the ethanol root bark extract of Cleistopholis patens (ERBECP) against doxorubicin-induced myocardial infarction in wistar rats. Extraction, preliminary phytochemical analysis, acute toxicity study and body weight (b.w.) of ERBECP were achieved using standard methods. Phyto-constituents in ERBECP were indentified using Gas Chromatography-Mass Spectrometry (GC–MS) technique. Thirty (30) male albino Wistar rats of average b.w. ranging between 100 and 130 g were divided into six groups of five rats each. Groups I, II and III served as normal, doxorubicin (DOX) and standard (Vasoprin 150 mg/kg b.w) controls respectively, while groups IV, V and VI were orally pre-treated with the extract (200, 400 and 600 mg/kgb.w) for two weeks prior to intraperitoneal induction of cardiotoxicity with DOX (20 mg/kg bw) on day 14. Results: Disturbances in serum cardiac function bio-markers such as; Cardiac Troponin-I (CTnI), Creatine Kinase (CK), Lactate Dehydrogenase (LDH), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT). Lipid profile markers such as; Total cholesterol (TC), Triacylglycerol (TAG), Low Density Lipoprotein (LDL), High Density Lipoprotein (HDL). Oxidative stress markers such as; Malondialdehyde (MDA), Superoxide Dismutase (SOD), Catalase (CAT), Glutathione (GSH) confirmed the induction of myocardial infarction. Histological assessment of heart tissues was performed to validate biochemical results. The GC–MS analysis of ERBECP identified a total of 69 compounds. Safety profile of the aqueous extract was safe for the animals up to the highest dose of 5000 mg/kg b.w. Pre-treatment of DOX group with ERBECP could significantly increase the b.w. compared to the DOX-treated group during the experimental period of 2 weeks. There were significant (p < 0.05) alterations in the levels of CTnI, CK, LDH, AST, ALT and lipid profile indices in the DOX control rats. Also, significant (p < 0.05) increase was observed in MDA and decrease in SOD, CAT and GSH in the DOX control rats. However, administration of the extract significantly (p < 0.05) normalized these alterations and reversed the architectural changes in the heart. The 69 compounds were screened against the target protein (CBR1); we identified seven hits based on the docking score and interactions with the active site residues. All the C. patens constituents had MW (g/mol) less than 500, HBA < 10 and HBD not more than 5. Apart, 9-Octadecenoic acid (Z)-, 2,3-dihydroxy propyl ester and Estra-1,3,5(10)-trien-17. beta. -ol, all the constituents had LD50 lower than 2000 mg/kg. Conclusions: The findings reveals ERBECP demonstrated promising potential and can be exploited in the development novel cardiac therapeutic agents. [ABSTRACT FROM AUTHOR]

Key points The sympathetic nervous system modulates cardiac contractile and electrophysiological function and contributes to adverse remodelling following myocardial infarction (MI). Axonal modulation therapy (AMT), directed at the sympathetic chain, blocks efferent sympathetic outflow to the heart and is a strategy to transiently and controllably mitigate chronic MI‐associated sympatho‐excitation. In porcine models, we evaluated scalable AMT, directed at the paravertebral chain, in blocking reflex‐mediated pacing‐induced sympatho‐excitation post‐MI. The level of sympatho‐excitation was assessed by dynamic interstitial measurement of noradrenaline (NA) and neuropeptide Y (NPY). In anaesthetized normal (n = 5) and age‐matched pigs 6 weeks post‐MI induction (n = 10), we electrically stimulated the right sympathetic chain and determined levels of direct current block applied at the T1–T2 level sufficient to reduce the evoked changes in heart rate and/or contractility by 25–75%. Reflex‐mediated neural release of NA and NPY into the interstitial space during programmed pacing (PP) was assessed using fast‐scanning cyclic voltammetry and capacitive immunoprobes. Normal animals demonstrated homogeneous NA and NPY release profiles during PP. In contrast, for MI animals PP evoked differential NA and NPY release in remote and MI border zones of the left ventricle. Right‐sided AMT mitigated NA and NPY pacing‐induced release in the remote left ventricle with a positive correlation to increasing AMT levels. Pacing‐induced NA and NPY release in the MI border zone was not mitigated by AMT. Differential effects of AMT on NA and NPY may underlie the anti‐arrhythmic effects of partial stellate ganglion block in the setting of chronic MI. Programmed cardiac pacing evokes homogeneous noradrenaline (NA) and neuropeptide Y (NPY) release in equivalent areas (e.g. medial and lateral aspects) of the normal left ventricle. Programmed cardiac pacing evokes differential NA and NPY release in remote and border zones of the infarcted left ventricle. Axonal modulation therapy (AMT), using a graded direct current block applied to the stellate ganglia, can proportionally modulate cardiac sympathetic reflexes. Unilateral AMT mitigates NA and NPY release in remote left ventricular tissue, with release negatively correlated to increasing AMT levels. Heterogeneities in NA and NPY between the border and remote tissues are reduced by progressive AMT. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) is a leading cause of heart failure, disability and mortality worldwide. In this study, the effects of intramyocardial injection of human platelet lysate (HPL), bone marrow mesenchymal stem cells pretreated with HPL (PMSCs), and PMSC lysate (lys), alone and in combination were investigated on MI-induced by LAD ligation in male Wistar rats. The experiment was carried out on sham, vehicle (Veh), HPL, PMSCs, PMSC lysate (PMSC lys), HPL + PMSCs, and HPL + PMSC lys groups. SBP, DBP, and ± dp/dt max were monitored by the PowerLab physiograph. The MSC characteristics and CD31, NKX2.5, and cardiac troponin I (cTnI) contents were determined by flow cytometry, immunohistochemistry, and immunofluorescence, respectively. SBP, DBP, and ± dp/dt max that decreased in the MI group were recovered by HPL, PMSC, PMSC lys, HPL + PMSC, and HPL + PMSC lys treatments. CD31 density was higher in all treated groups compared to the Veh group. CD31 density in the HPL + PMSCs and HPL + PMSC lys groups was higher than in the PMSCs group. The number of Dil+/NKX2.5 + and Dil+/cTnI + cells was higher in the HPL + PMSCs group compared to the PMSCs group. The HPL and PMSCs mitigates heart injuries and cardiac dysfunction after MI. HPL provides an appropriate environment for cardiomyocyte differentiation from PMSCs. [ABSTRACT FROM AUTHOR]

Background: Previous literature has explored the relationship between television viewing and cardiovascular disease (CVD) in adults; however, there remains a paucity of longitudinal data describing how young adult television viewing relates to premature CVD events. Objective: To ascertain the relationship between level and annualized changes in television viewing from young adulthood to middle age and the incidence of premature CVD events before age 60. Design: The Coronary Artery Risk Development in Young Adults (CARDIA) study, a prospective community-based cohort with over 30 years of follow-up (1985–present). Participants: Black and White men and women who were 18–30 years old at baseline (1985–1986). Main Measures: Independent variables: Individualized television viewing trajectories were developed using linear mixed models. Dependent variables: Fatal and nonfatal coronary heart disease (CHD), heart failure, and stroke outcomes were analyzed separately and as a combined CVD event outcome. Key Results: Among 4318 included participants, every 1-h increase in daily hours of television viewing at age 23 was associated with higher odds of incident CHD (adjusted odds ratio [AOR] 1.26, 95% confidence interval [CI] 1.06–1.49) and incident CVD events (AOR 1.16, 95% CI 1.03–1.32). Each additional hour of daily television viewing annually was associated with higher annual odds of CHD incidence (AOR 1.55, 95% CI 1.06–2.25), stroke incidence (AOR 1.58, 95% CI 1.02–2.46), and CVD incidence (AOR 1.32, 95% CI 1.03–1.69). Race and sex modified the association between television viewing level at age 23 and CHD, heart failure, and stroke, with White men most consistently having significant associations. Conclusions: In this prospective cohort study, greater television viewing in young adulthood and annual increases in television viewing across midlife were associated with incident premature CVD events, particularly CHD. Young adulthood as well as behaviors across midlife may be important periods to promote healthy television viewing behavior patterns. [ABSTRACT FROM AUTHOR]

Cardiovascular disease such as myocardial infarction is one of the chief reasons for death universally. An extensive variety of natural and synthetic biodegradable polymers have been studied lately for cardiac tissue engineering applications. Cardiac tissue regeneration is a substitute approach for in situ cellular cardiomyoplasties, which is considered to renovate infarcted myocardium utilizing cells, scaffold, and growth factors. Polymer-based scaffolds including graphene and carbon nanotubes can be employed for heart tissue engineering. In this review, we consider the literature in terms of cardiac tissue engineering and discuss the most recent developments in terms of scaffold-based polymers for cardiac tissue regeneration. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) is a leading cause of heart failure, disability and mortality worldwide. In this study, the effects of intramyocardial injection of human platelet lysate (HPL), bone marrow mesenchymal stem cells pretreated with HPL (PMSCs), and PMSC lysate (lys), alone and in combination were investigated on MI-induced by LAD ligation in male Wistar rats. The experiment was carried out on sham, vehicle (Veh), HPL, PMSCs, PMSC lysate (PMSC lys), HPL + PMSCs, and HPL + PMSC lys groups. SBP, DBP, and ± dp/dt max were monitored by the PowerLab physiograph. The MSC characteristics and CD31, NKX2.5, and cardiac troponin I (cTnI) contents were determined by flow cytometry, immunohistochemistry, and immunofluorescence, respectively. SBP, DBP, and ± dp/dt max that decreased in the MI group were recovered by HPL, PMSC, PMSC lys, HPL + PMSC, and HPL + PMSC lys treatments. CD31 density was higher in all treated groups compared to the Veh group. CD31 density in the HPL + PMSCs and HPL + PMSC lys groups was higher than in the PMSCs group. The number of Dil+/NKX2.5 + and Dil+/cTnI + cells was higher in the HPL + PMSCs group compared to the PMSCs group. The HPL and PMSCs mitigates heart injuries and cardiac dysfunction after MI. HPL provides an appropriate environment for cardiomyocyte differentiation from PMSCs. [ABSTRACT FROM AUTHOR]

Background: Although stem cell transplantation is a promising approach for the treatment of myocardial infarction (MI), there are still some problems faced such as the low survival rate of stem cells. Here, we investigated the role of Notoginsenoside R1 (NGR1) pretreatment in improving the effects of neonatal rat bone marrow mesenchymal stem cell (MSC) transplantation for treatment of MI. Methods: Cardiac functions were detected by echocardiography and the myocardial infarct size was determined by Masson's trichrome staining in a rat model of MI. The cardioprotective effects of NGR1/LY294002 co-pretreated MSCs was evaluated to explore the underlying mechanism. The angiogenesis was determined by vWF and α-SMA immunofluorescence staining and cell apoptosis was detected by TUNEL. In vitro, the effects of NGR1 on stem cell proliferation was examined by CCK-8 and levels of P-Akt, P-CREB, P-FoxO1 were detected by western blot. Apoptosis, ROS content, and cytokine levels were examined by DAPI and TUNEL staining, a ROS assay kit, and ELISA, respectively. Results: NGR1 elevated the therapeutic effect of MSC transplantation on infarction by preserving cardiac function, increasing angiogenesis and expressions of IGF-1, VEGF, and SDF-1, and reducing cell apoptosis, whereas the addition of LY294002 prior to NGR1 treatment significantly counteracted the foregoing effects of NGR1. NGR1 pretreatment and SC79 pretreatment were similar in that both significantly increased P-Akt and P-FoxO1 levels in MSC and did not affect P-CREB levels. Besides, both NGR1 and SC79 promoted VEGF, SCF and bFGF levels in MSC cultures, and significantly reduced ROS accumulation and the attenuated cell apoptosis in MSC triggered by H2O2. Similarly, addition of LY294002 before NGR1 treatment significantly counteracted the aforementioned effects of NGR1 in vitro. Conclusions: NGR1 pretreatment enhances the effect of MSC transplantation for treatment of MI through paracrine signaling, and the mechanism underlying this effect may be associated with PI3K/Akt/FoxO1 signaling pathways. [ABSTRACT FROM AUTHOR]

Background: The efficiency of mesenchymal stem cells (MSCs) in treating myocardial infarction (MI) remains inconsistent, which limits their therapeutic applications. Therefore, exploring the mechanism for the inconsistent efficacy of MSCs and identification the criteria for screening MSCs are important for improving the efficiency of MSCs. Methods: Mouse model after MI was utilized to test the role of MSCs from different donors and the functional subpopulation in improving cardiac function. Heterogeneity of MSCs was identified using single-cell RNA sequencing (scRNA-seq) of MSC-GY. GSEA and Scissor analyses were used to find the functional subpopulations of MSCs that promote angiogenesis. The role of functional subpopulations in promoting angiogenesis was verified by detecting the secretory proteins, the ratio of N-CADHERIN+/CD168− subpopulations in MSCs, and the tube formation, migration, and proliferation of HUVECs after treatment with conditional medium (CM) derived from different MSCs. Results: We found that umbilical cord-derived MSCs (UC-MSCs) from different donors have varied therapeutic efficacy in MI mice and UC-MSCs with higher therapeutic effectiveness exhibited the most potent pro-angiogenic effects by secreting elevated levels of angiogenesis-related proteins, such as MYDGF, VEGFA, and FGF2. ScRNA-seq of 10,463 UC-MSCs revealed that the N-CADHERIN+/CD168− subpopulation was closely associated with pro-angiogenic effects, and the ratio of this cell subpopulation was positively correlated with the angiogenic potential of MSCs. We also found that the N-CADHERIN+/CD168− subpopulation was the functional subpopulation of MSCs in improving cardiac function of MI mice. Conclusions: Our study identified that the N-CADHERIN+/CD168− subpopulation was the functional subpopulation of MSCs in treating MI, which was essential for the development and utilization of MSCs in MI treatment. [ABSTRACT FROM AUTHOR]

Background and aims: About 50% of patients continue to smoke after stroke and myocardial infarction. We aimed to assess the effect of a multiple risk factor intervention on long-term smoking cessation and to explore a possible association between early smoking cessation and long-term prognosis. Material and methods: Consecutive patients with stroke/TIA/acute coronary syndrome (ACS) at Östersund Hospital during 2010–2014 were included, randomized to intervention or usual care (1:1), and followed through 2017. This substudy included participants that reported current smoking during hospitalization and were alive at 1 month post discharge when the intervention began (n = 321). The smoking cessation intervention was part of a telephone-based, multiple risk factor intervention delivered by a nurse and consisted of brief advice delivered annually. Smoking cessation at the last follow-up was analyzed as the primary outcome. Smoking cessation at other time points and association between early smoking cessation and prognosis (CV events, survival) were secondary outcomes. Result: After a mean follow-up of 4.2 years, 171 participants reported nonsmoking, with no significant difference between the intervention and control group (50.3% vs. 56.3%, absolute difference 5.9%, 95% CI −5.0 to 16.7, p = 0.286). Of these, 80.7% had stopped smoking within 1 month after discharge. The intervention did not improve smoking cessation proportions in the long or short term, and there was no apparent effect on smoking cessation attempts or sustained abstinence. Smoking cessation within 1 month was associated with lower all-cause mortality (HR 0.52, 95% CI 0.32–0.87), and there was a nonsignificant trend towards a lower incidence of CV events (HR 0.71, 95% CI 0.45–1.12). Conclusion: Annual brief advice by a nurse as part of a multiple risk factor follow-up did not improve long-term smoking cessation after stroke/TIA/ACS. Continued smoking past 1 month was associated with worse prognosis. Trial registration: ISRCTN registry ISRCTN96595458, ISRCTN23868518, ISRCTN30433343. [ABSTRACT FROM AUTHOR]

Objective Methods Results Conclusions Metabolic dysfunction‐associated steatotic liver disease (MASLD) and obesity increases risk of cardiovascular disease. This cohort study examines the prognostic value of MASLD, across body weight categories, in a secondary preventative acute myocardial infarction (AMI) cohort.Patients with AMI were stratified into four phenotypes—obesity MASLD, non‐obesity MASLD, obesity non‐MASLD, non‐obesity non‐MASLD. The primary outcome was all‐cause mortality. Cox regression analysis was performed to investigate determinants of long‐term all‐cause mortality.Of 5702 patients, majority were in the non‐obesity non‐MASLD group (66.7%), followed by obesity MASLD (16.1%), non‐obesity MASLD (11.2%) and non‐obesity MASLD (6.0%). Across the four phenotypes, obesity MASLD had the highest cardiometabolic burden, followed by non‐obesity MASLD. Non‐obesity MASLD had the highest risk of heart failure (p = 0.034), cardiogenic shock (p < 0.001), and all‐cause long‐term mortality (p = 0.019). The non‐obesity MASLD (HR 1.400, 95%CI 1.077–1.820, p = 0.012) and obesity MASLD phenotypes (HR 1.222, 95%CI 1.005–1.485, p = 0.044) were independently associated with long‐term all‐cause mortality.Obesity and non‐obesity MASLD phenotypes were predictors of all‐cause mortality following AMI, with an even larger magnitude of mortality risk in the non‐obesity MASLD group. The recognition of MASLD and its body weight phenotypes will be beneficial in the prognostication following AMI. [ABSTRACT FROM AUTHOR]

The effectiveness of complete revascularization is well established in patients with ST-segment elevation myocardial infarction (STEMI), but it is less investigated in those with non–ST-segment elevation myocardial infarction (NSTEMI). This study aimed to assess whether complete revascularization, compared with culprit-only revascularization, was associated with consistent outcomes in older patients with STEMI and NSTEMI. In the FIRE (Functional Assessment in Elderly MI Patients with Multivessel Disease) trial, 1,445 older patients with myocardial infarction (MI) were randomized to culprit-only or physiology-guided complete revascularization, stratified by STEMI (n = 256 culprit-only vs n = 253 complete) and NSTEMI (n = 469 culprit-only vs n = 467 complete). The primary outcome comprised a composite of death, MI, stroke, or revascularization at 1 year. The key secondary outcome included a composite of cardiovascular death or MI at 1 year. In the overall study population, physiology-guided complete revascularization reduced both primary and key secondary outcomes. The primary outcome occurred in 54 (21.1%) STEMI patients randomized to culprit-only vs 41 (16.2%) STEMI patients of the complete group (HR: 0.75; 95% CI: 0.50-1.13) and in 98 (20.9%) NSTEMI patients randomized to culprit-only vs 72 (15.4%) NSTEMI patients of the complete group (HR: 0.71; 95% CI: 0.53-0.97), with negative interaction testing (P for interaction, 0.846). Similarly, no signal of heterogeneity with respect to the initial clinical presentation was observed for the key secondary endpoint (P for interaction, 0.654). Physiology-guided complete revascularization, compared with culprit-only revascularization, provided consistent benefit across the whole spectrum of patients with MI. (FIRE [Functional Assessment in Elderly MI Patients With Multivessel Disease]; NCT03772743) [ABSTRACT FROM AUTHOR]

Background: The clinical application of mesenchymal stem cells (MSCs) in myocardial infarction (MI) is severely hampered by their poor survival. Pretreatment is a key strategy that has been adopted to promote their therapeutic efficacy. This study aimed to investigate the benefit of growth differentiation factor 15-pretreated MSCs (GDF15-MSCs) in enhancing cardiac repair following MI and to determine the underlying mechanisms. Methods: MSCs with or without GDF15 pretreatment were exposed to serum deprivation and hypoxia (SD/H) challenge. Apoptosis of MSCs was assessed by TUNEL staining. The conditioned media (CM) of MSCs and GDF15-MSCs was collected by centrifugation. MSCs and GDF15-MSCs were transplanted into the peri-infarct region in a mouse model of MI. Cardiac function, fibrosis and MSC survival were examined 4 weeks after MSC transplantation. Results: Pretreatment with GDF15 greatly reduced SD/H-induced apoptosis of MSCs via inhibition of reactive oxygen species (ROS) generation by attenuating mitochondrial fission. Mechanistically, GDF15 pretreatment ameliorated mitochondrial fission of MSCs under SD/H challenge by activating the AMPK pathway. These effects were partially abrogated by AMPK inhibitor. Pretreatment with GDF15 also promoted paracrine effects of MSCs in vitro, evidenced by improving tube formation of HUVECs, and inhibited the apoptosis of cardiomyocytes induced by SD/H. At 4 weeks after transplantation, compared with MSCs, GDF15 pretreatment strongly promoted the survival of MSCs in the ischemic heart with consequent enhanced cardiac function, reduced cardiac fibrosis and increased angiogenesis. Conclusions: Our study showed that pretreatment with GDF15 promoted the cardioprotective effects of MSCs in MI via regulation of pro-survival signaling and paracrine actions. GDF15 pretreatment is an effective approach to enhance the therapeutic efficacy of MSCs in ischemic heart disease. [ABSTRACT FROM AUTHOR]

Background: Progranulin is a secreted glycoprotein that regulates inflammation and wound healing. However, plasma progranulin levels in the acute phase and their clinical significance in patients with acute myocardial infarction (AMI) remain to be elucidated. Objective: We aimed to investigate the relationship between the increase in plasma progranulin levels in the acute phase and the recovery of left ventricular function in the chronic phase in AMI patients. Method and result: Eighteen AMI patients were followed up for 6 months. Blood samples were collected from the antecubital vein on day 0 (on admission) and day 7 in the acute phase. The control group consisted of patients without significant coronary artery stenosis, as assessed by cardiac catheterization (n = 16). Plasma progranulin levels were measured by enzyme-linked immunosorbent assay. Echocardiography was performed in the acute (within 7 days) and chronic (6 months) phases of AMI to evaluate left ventricular ejection fraction using the modified Simpson's method. Plasma progranulin levels in the AMI group on day 0 (69.5 ± 24.6 ng/mL) were similar to those in the control group (84.2 ± 47.1 ng/mL). There was a significant increase in progranulin levels in the AMI group on day 7 (104.2 ± 52.0 ng/mL) compared with day 0. The increase in plasma progranulin levels in the acute phase was positively correlated with the increase in left ventricular ejection fraction between the acute and chronic phases. Among various factors, only plasma progranulin levels were favorably correlated with left ventricular functional recovery in the chronic phase. Conclusion: The increase in plasma progranulin levels in the acute phase may serve as a predictive biomarker and a contributer for the recovery of left ventricular function in the chronic phase in patients with AMI. [ABSTRACT FROM AUTHOR]

ABSTRACT Aim Background Methods Results Conclusion Relevance to Clinical Practice Patient or Public Contribution To examine the relationship between health literacy with the quality of discharge planning and readiness for hospital discharge in acute myocardial infarction patients in Jordan.Acute myocardial infarction is a major heart disease caused by plaque formation in coronary arteries. Complications after acute myocardial infarction include readmission and physical complications such as chest pain, and limited health literacy increases the risk of complications. Improving the health literacy of patients can improve postdischarge outcomes and decrease complications.This study was conducted using a cross‐sectional design. Data were collected from 123 patients who were recruited from three hospitals in Jordan. A demographics questionnaire and three valid and reliable instruments (Health Literacy Questionnaire, Readiness for Hospital Discharge Scale and Quality of Discharge Teaching Scale) were used to collect the data. The authors adhered to the STROBE checklist during the preparation of this study.The results demonstrated that the Readiness for Hospital Discharge had weak to moderate positive correlations with health literacy scales (r = 0.24–0.36, p < 0.05). The content subscale of the Quality of Discharge Teaching Scale showed weak positive correlations with navigating the healthcare system, finding good health information and understanding health information scales of the Health Literacy Questionnaire.The results reported here indicate that health literacy positively correlates with readiness for hospital discharge and quality of discharge teaching.Improving the health literacy of acute myocardial infarction patients can enhance their discharge planning outcomes. The findings of this study are beneficial for healthcare providers in designing targeted interventions that correspond to health literacy among acute myocardial infarction patients.No patient or public contribution. [ABSTRACT FROM AUTHOR]

BACKGROUND Whether a conservative strategy of medical therapy alone or a strategy of medical therapy plus invasive treatment is more beneficial in older adults with non-ST-segment elevation myocardial infarction (NSTEMI) remains unclear. METHODS We conducted a prospective, multicenter, randomized trial involving patients 75 years of age or older with NSTEMI at 48 sites in the United Kingdom. The patients were assigned in a 1:1 ratio to a conservative strategy of the best available medical therapy or an invasive strategy of coronary angiography and revascularization plus the best available medical therapy. Patients who were frail or had a high burden of coexisting conditions were eligible. The primary outcome was a composite of death from cardiovascular causes (cardiovascular death) or nonfatal myocardial infarction assessed in a time-to-event analysis. RESULTS A total of 1518 patients underwent randomization; 753 patients were assigned to the invasive-strategy group and 765 to the conservative-strategy group. The mean age of the patients was 82 years, 45% were women, and 32% were frail. A primary-outcome event occurred in 193 patients (25.6%) in the invasive-strategy group and 201 patients (26.3%) in the conservative-strategy group (hazard ratio, 0.94; 95% confidence interval [CI], 0.77 to 1.14; P = 0.53) over a median follow-up of 4.1 years. Cardiovascular death occurred in 15.8% of the patients in the invasive-strategy group and 14.2% of the patients in the conservative-strategy group (hazard ratio, 1.11; 95% CI, 0.86 to 1.44). Nonfatal myocardial infarction occurred in 11.7% in the invasive-strategy group and 15.0% in the conservative-strategy group (hazard ratio, 0.75; 95% CI, 0.57 to 0.99). Procedural complications occurred in less than 1% of the patients. CONCLUSIONS In older adults with NSTEMI, an invasive strategy did not result in a significantly lower risk of cardiovascular death or nonfatal myocardial infarction (the composite primary outcome) than a conservative strategy over a median follow-up of 4.1 years. (Funded by the British Heart Foundation; BHF SENIOR-RITA ISRCTN Registry number, ISRCTN11343602.). [ABSTRACT FROM AUTHOR]

Familial hypercholesterolemia (FH) is a world public health problem that enhances the risk of premature coronary artery disease (CAD) with a high incidence of acute coronary syndrome. This study aimed to evaluate the clinical and angiographic characteristics of the patients with and without FH who had ST-elevation myocardial infarction (STEMI). It included 690 patients who presented with the first attack of STEMI and underwent primary percutaneous coronary interventions (PPCI). The patients were analyzed to diagnose FH according to the Dutch Lipid Clinic Network (DLCN) criteria. All angiograms were analyzed for the number of diseased vessels, Syntax score, thrombus burden grade, and final Thrombolysis in Myocardial Infarction (TIMI) flow grade. The majority of patients were male (72.6%) with a mean age of 54 ± 12 years. Based on DLCN criteria, they were classified into unlikely/possible FH (86.1%) and probable/definite FH (13.9%) groups. Probable/definite FH patients were significantly younger, and higher incidence of males < 55 years compared with unlikely/possible FH patients (p < 0.001 for each). Moreover, probable/definite FH patients had a higher frequency of three-vessel disease (p = 0.007) and Syntax score (p < 0.001) with a moderate positive correlation with the DLCN score (r = 0.592, p < 0.001). Furthermore, probable/definite FH patients showed a higher thrombus burden and final TIMI slow/no-reflow when compared to the unlikely/possible FH patients (p = 0.006 and p = 0.027, respectively). Patients with probable/definite FH and LDL-C level were independent predictors of high thrombus burden besides males < 55 years, and the number of diseased vessels. In conclusion, STEMI patients with FH were younger males and associated with severe CAD with frequent multivessel CAD, high anatomical complexity of CAD, and frequent high thrombus burden. Furthermore, FH was one of the predictors of high thrombus burden. [ABSTRACT FROM AUTHOR]

Background: In older adults with hypertension, hip fractures accompanied by preoperative acute heart failure significantly elevate surgical risks and adverse outcomes, necessitating timely identification and management to improve patient outcomes. Research objective: This study aims to enhance the early recognition of acute heart failure in older hypertensive adults prior to hip fracture surgery by developing a predictive model using logistic regression (LR) and machine learning methods, optimizing preoperative assessment and management. Methods: Employing a retrospective study design, we analyzed hypertensive older adults who underwent hip fracture surgery at Hebei Medical University Third Hospital from January 2018 to December 2022. Predictive models were constructed using LASSO regression and multivariable logistic regression, evaluated via nomogram charts. Five additional machine learning methods were utilized, with variable importance assessed using SHAP values and the impact of key variables evaluated through multivariate correlation analysis and interaction effects. Results: The study included 1,370 patients. LASSO regression selected 18 key variables, including sex, age, coronary heart disease, pulmonary infection, ventricular arrhythmias, acute myocardial infarction, and anemia. The logistic regression model demonstrated robust performance with an AUC of 0.753. Although other models outperformed it in sensitivity and F1 score, logistic regression's discriminative ability was significant for clinical decision-making. The Gradient Boosting Machine model, notable for a sensitivity of 95.2%, indicated substantial capability in identifying patients at risk, crucial for reducing missed diagnoses. Conclusion: We developed and compared efficacy of predictive models using logistic regression and machine learning, interpreting them with SHAP values and analyzing key variable interactions. This offers a scientific basis for assessing preoperative heart failure risk in older adults with hypertension and hip fractures, providing significant guidance for individualized treatment strategies and underscoring the value of applying machine learning in clinical settings. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases are a cause of death making it crucial to accurately diagnose them. Electrocardiography plays a role in detecting heart issues such as heart attacks, bundle branch blocks and irregular heart rhythms. Manual analysis of ECGs is prone to mistakes and time consuming, underscoring the importance of automated methods. This study uses AI models like AlexNet and a dual branch model for categorizing ECG signals from the PTB Diagnostic ECG Database. AlexNet achieved a validation accuracy of 98.64% and a test set accuracy of 99% while the dual branch fusion network model achieved a test set accuracy of 99%. Data preprocessing involved standardizing, balancing and reshaping ECG signals. These models exhibited precision, sensitivity and specificity. In comparison to state of the arts' models such as Hybrid AlexNet SVM and DCNN LSTM our proposed models displayed performance. The high accuracy rates of 99% underscore their potential for ECG classification. These results validate the advantages of incorporating learning models into setups for automated ECG analysis providing adaptable solutions for various healthcare settings including rural areas. [ABSTRACT FROM AUTHOR]

Despite the widespread adoption of emergency coronary reperfusion therapy, reperfusion‐induced myocardial injury remains a challenging issue in clinical practice. Following myocardial reperfusion, S100A8/A9 molecules are considered pivotal in initiating and regulating tissue inflammatory damage. Effectively reducing the S100A8/A9 level in ischemic myocardial tissue holds significant therapeutic value in salvaging damaged myocardium. In this study, HA (hemagglutinin)‐ and RAGE (receptor for advanced glycation end products)‐ comodified macrophage membrane‐coated siRNA nanoparticles (MMM/RNA NPs) with siRNA targeting S100A9 (S100A9‐siRNA) are successfully prepared. This nanocarrier system is able to target effectively the injured myocardium in an inflammatory environment while evading digestive damage by lysosomes. In vivo, migration of MMM/RNA NPs to myocardial injury lesions is confirmed in a myocardial ischemia‐reperfusion injury (MIRI) mouse model. Intravenous injection of MMM/RNA NPs significantly reduced S100A9 levels in serum and myocardial tissues, further decreasing myocardial infarction area and improving cardiac function. Targeted reduction of S100A8/A9 by genetically modified macrophage membrane‐coated nanoparticles may represent a new therapeutic intervention for MIRI. [ABSTRACT FROM AUTHOR]

18F-GP1 is a novel highly specific radiotracer that binds to activated platelets and thrombus. We aimed to establish the observer repeatability of coronary, carotid and cerebral 18F-GP1 uptake in patients presenting with acute myocardial infarction or ischaemic stroke. Forty-three patients presenting with acute myocardial infarction or ischaemic stroke underwent hybrid positron emission tomography (PET) and computed tomography (CT) angiography. Qualitative and quantitative assessment of 18F-GP1 uptake was performed on coronary arteries, carotid arteries and brain parenchyma. Qualitative uptake of 18F-GP1 had excellent intraobserver and interobserver agreement, with complete agreement for the presence or absence of visual 18F-GP1 uptake. For quantitative analysis, there were excellent intraclass correlation coefficients for intraobserver repeatability for coronary artery, carotid artery and brain parenchymal SUVmax and TBRmax measurements (all ≥ 0.92). Coronary artery and brain parenchymal analyses showed the strongest agreement in SUVmax values with mean biases of − 0.04 (limits of agreement − 0.21 to 0.20) and 0.02 (limits of agreement − 0.29 to 0.32) respectively. There was good interclass correlation coefficients for interobserver repeatability for coronary artery, carotid artery and brain parenchymal SUVmax and TBRmax measurements (all ≥ 0.89). The strongest interobserver agreement was seen with brain parenchymal SUVmax (mean SUVmax 1.95 ± 0.94) and TBRmax (mean TBRmax 9.55 ± 6.56) with mean biases of − 0.05 (limits of agreement − 0.37 to 0.27) and 0.04 (limits of agreement − 0.59 to 0.52) respectively. Visual qualitative and quantitative 18F-GP1 PET-CT image analyses provide robust and repeatable measurements of activated platelets and thrombi within the coronary arteries, carotid arteries and brain parenchyma. [ABSTRACT FROM AUTHOR]

Background: Inflammation and neurohormonal activation play a significant role in the adverse outcome seen in acute myocardial infarction (AMI) and the development of cardiogenic shock (CS), which is associated with a mortality rate up to 50%. Treatment with anti-inflammatory drugs such as tocilizumab, an interleukin-6 receptor antagonist, has been shown to reduce troponin release and reduce the myocardial infarct size in AMI patients and it may therefore have cardioprotective properties. Methods: This is a double-blind, placebo-controlled, single-center randomized clinical trial, including adult AMI patients without CS at hospital arrival, undergoing percutaneous coronary intervention (PCI) within 24 h from symptom onset, and at intermediate to high risk of developing CS (ORBI risk score ≥ 10). A total of 100 participants will be randomized to receive a single intravenous dose of tocilizumab (280 mg) or placebo (normal saline). The primary outcome is peak plasma pro-B-type natriuretic peptide (proBNP) within 48 h, assessed using serial measurements at intervals: before infusion, 12, 24, 36, and 48 h after infusion. Secondary endpoints include the following: (1) cardiac magnetic resonance imaging (CMR) during 24–48 h after admission and at follow-up after 3 months with assessment of left ventricular area at risk, final infarct size, and the derived salvage index and (2) biochemical markers of inflammation (C-reactive protein and leukocyte counts) and cardiac injury (troponin T and creatinine kinase MB). Discussion: Modulation of interleukin-6-mediated inflammation in patients with AMI, treated with acute PCI, and at intermediate to high risk of in-hospital CS may lead to increased hemodynamic stability and reduced left ventricular infarct size, which will be assessed using blood biomarkers with proBNP as the primary outcome and inflammatory markers, troponin T, and CMR with myocardial salvage index as the secondary endpoints. Trial registration: Registered with the Regional Ethics Committee (H-21045751), EudraCT (2021–002028-19), ClinicalTrials.gov (NCT05350592). Study registration date: 2022-03-08, Universal Trial Number U1111-1277–8523. [ABSTRACT FROM AUTHOR]

The study's goals are to fabricate PLGA nanoparticles (PNPs) loaded with apigenin (AP) and adenosine (AD) using a microfluidic preparation method to a standard emulsification method and investigate the possible heart-protective effects of AP-AD PNPs made using the emulsification method. Compared to microfluidics, the emulsification method fabricated small-size nanoparticles, which are better at encapsulating drugs, retaining more drugs, and having a low viscosity for the myocardial infarction (MI) injection. TheMI model was developed using SD rats injected under the skin with 85 mg/kg doxorubicin (DOX) for 2 days. The metabolic results showed that our AP-AD PNPs accelerated the blood flow in rats with MI, which increased the amounts of AP and AD in the circulatory system. This led to significant improvements in the cardiac index and lower amounts of AST, LDH, and CK in the blood. A histopathological study using Hematoxylin&eosin, and TUNEL staining showed that cardiac function had improved and apoptosis had decreased. Moreover, tests that checked the amounts of IL-6, TNF-α, NO, GSH, MDA, and SOD showed that AP-AD PNPs may help treat MI by reducing oxidative stress and inflammation, making it a potentially useful therapeutic approach. [ABSTRACT FROM AUTHOR]

Cardiac troponin I (cTnI) is the most resorted biomarker for the detection of cardiovascular disease (CVD). The means of rapid quantification of cTnI levels in the blood can substantially minimize the risk of acute myocardial infarction and heart failure. A sensor for the non‐enzymatic evaluation of cardiac troponin‐I has been developed using fluorescent iron nanoclusters via a one‐pot synthesis employing (BSA) as the template and reducing agent, and hydrogen peroxide as the additive. The fluorescence of Iron Nanocluster is quenched with graphene oxide (GO) via fluorescence resonance energy transfer (FRET) between conjugate iron nanoclusters and graphene oxide. The sensor shows a low detection limit of 0.011 ng/mL. The benefits of utilizing a non‐enzymatic probe for detecting cardiac troponin I is that it avoids the need for enzymes and hence is economical, stable, and less impacted by environmental conditions such as temperature and pH. Non‐enzymatic probes are more useful for clinical use since they are more stable and have a longer shelf life. The developed non‐enzymatic probes are also highly selective and sensitive to the target analyte, making them suitable for the direct detection of cardiac troponin I in actual biological samples. [ABSTRACT FROM AUTHOR]

The prevalence of cardiometabolic morbidity (e.g., high blood pressure, heart attack, stroke, type 2 diabetes) and multimorbidity development (2 or more cardiometabolic morbidities) are rapidly growing in the US. Cardiometabolic morbidity and multimorbidity are linked to poor well‐being outcomes, high healthcare costs, and mortality. There is little known about cardiometabolic multimorbidity health disparities, particularly regarding mutable factors that might be targeted in future health interventions. In the present study, using a biopsychosocial framework (Biobehavioral Family Model), we examine whether cardiometabolic morbidity and multimorbidity development are linked to premorbid family and marital relationships and if it differs depending on socioeconomic status (i.e., educational attainment) using three waves of Midlife in the US (N = 4951). We assessed cardiometabolic development with three conceptualizations: number of cardiometabolic morbidities (i.e., count variable), individual cardiometabolic morbidities (i.e., diabetes, high blood pressure, stroke, heart attack), and severity of cardiometabolic multimorbidity (e.g., 3+ vs. zero morbidities). Family strain increased the number of cardiometabolic morbidities (OR = 1.17) and the severity of multimorbidity (e.g., 3+ morbidities: OR = 1.38). People with a high school education experienced family support as a buffer to the negative health impact of education level. Generally, marital quality appeared less impactful on cardiometabolic morbidity and multimorbidity development compared to family strain. Positive and negative family characteristics appear to function differently across educational attainment. These findings indicate that adults’ non‐intimate family relationships predict important outcomes such as diabetes, heart attack, stroke, and cardiometabolic multimorbidity and should be considered targets for preventative health interventions. [ABSTRACT FROM AUTHOR]

A novel immunoassay platform is presented utilizing a cardiac troponin T antibody (Ab-cTnT) labelled with 5-carboxyfluorescein (5-FAM) integrated into a two-dimensional (2D) manganese dioxide nanosheet (MnO2 NS) matrix. This strategy enables a turn-on response towards cTnT antigen within a mere 10-min incubation period, boasting an impressive lower detection limit of 0.038 ng/mL. Crucially, our probe demonstrates exceptional selectivity amidst the presence of coexisting biomolecules and ions, ensuring precise detection of cTnT. Moreover, the developed platform showcases promising utility in sensing cTnT from spiked human serum samples, yielding satisfactory recovery percentages ranging from 82 to 105%. Additionally, we introduce and easy-to-use and cost-effective test strip for point-of-care detection of cTnT, further enhancing accessibility to critical cardiovascular diagnostics. [ABSTRACT FROM AUTHOR]

Heart failure (HF) remains prevalent in patients who survived myocardial infarction (MI). Despite the accessibility of the primary percutaneous coronary intervention and medications that alleviate ventricular remodeling with functional improvement, there is an urgent need for clinicians and basic scientists to further reveal the mechanisms behind post‐MI HF as well as investigate earlier and more efficient treatment after MI. Growing numbers of studies have highlighted the crucial role of macrophages in cardiac repair and remodeling following MI, and timely intervention targeting the immune response via macrophages may represent a promising therapeutic avenue. Recently, technology such as single‐cell sequencing has provided us with an updated and in‐depth understanding of the role of macrophages in MI. Meanwhile, the development of biomaterials has made it possible for macrophage‐targeted therapy. Thus, an overall and thorough understanding of the role of macrophages in post‐MI HF and the current development status of macrophage‐based therapy will assist in the further study and development of macrophage‐targeted treatment for post‐infarction cardiac remodeling. This review synthesizes the spatiotemporal dynamics, function, mechanism and signaling of macrophages in the process of HF after MI, as well as discusses the emerging bio‐materials and possible therapeutic agents targeting macrophages for post‐MI HF. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cell (MSC)‐derived extracellular vesicles (EVs) are a promising treatment for myocardial infarction (MI), but their therapeutic efficacy is limited by inefficient accumulation at the target site. A minimally invasive MSC EV therapy that enhances EV accumulation at the disease site and extends EV retention could significantly improve post‐infarct cardiac regeneration. Here, we show that EVs decorated with the next‐generation of high‐affinity (HiA) heterodimerizing leucine zippers, termed HiA Zippersomes, amplify targetable surface areas through in situ crosslinking and exhibited ~7‐fold enhanced accumulation within the infarcted myocardium in mice after 3 days and continued to be retained up to Day 21, surpassing the performance of unmodified EVs. After MI in mice, HiA Zippersomes increase the ejection fraction by 53% and 100% compared with unmodified EVs and phosphate‐buffered saline (PBS), respectively. This notable improvement in cardiac function played a crucial role in restoring healthy heart performance. HiA Zippersomes also robustly decrease infarct size by 52% and 60% compared with unmodified EVs and PBS, respectively, thus representing a promising platform for minimally invasive vesicle delivery to the infarcted heart compared to intramyocardial injections. [ABSTRACT FROM AUTHOR]

This study evaluated the role of the mesenchymal stem cells derived from adipose tissue (MSCs) in provoked ventricular arrhythmias (VAs) in animals with myocardial infarction (MI). The experimental groups were: sham, subjected to sham surgery and intramyocardial saline injection; MIV, infarcted rats subjected to intramyocardial saline injection; MI + MSCs, infarcted rats subjected to intramyocardial MSCs injection. Injections were performed two days after infarction and the arrhythmogenic inducibility experiment was performed the next day. Only 35% of the MI + MSCs group developed VAs, while the one in the MIV group was 65%. The proportion of nonsustained ventricular tachycardia, sustained tachycardia, and ventricular fibrillation was similar between the infarcted groups, but MSCs animals had shorter duration of nonsustained ventricular tachycardia. However, MSCs increased connexin 43 content in the remote area, even above the levels found in the sham group. MSCs prevented the increase of IL-1β in the different areas of the myocardium. There was higher carbonylation and content of 4-hydroxynonenal (4-HNE, a marker of lipoperoxidation) in the myocardium of infarcted rats, but MSCs attenuated the increase of 4-HNE in the infarcted area. In conclusion, MSCs have a protective effect against the development of arrhythmias, but do not imply a significant benefit for animals that have developed VAs. It is possible to think that the cardioprotection of MSCs involves anti-inflammatory/oxidative actions and improvement in the formation of communicating junctions. Graphical abstract [ABSTRACT FROM AUTHOR]

Although observational studies have linked primary aldosteronism (PA) with cardiovascular diseases (CVDs), the causality remains uncertain. In this study, we aimed to investigate whether PA is causally associated with CVD risk and cardiac magnetic resonance (CMR) parameters using the Mendelian randomization (MR) method. Independent and genome‐wide significant single nucleotide polymorphisms for PA were extracted from genome‐wide association study (GWAS) summary statistics. Genetic associations with the CVDs and CMR parameters were obtained from recent large‐scale GWASs or genetic consortia. Inverse‐variance weighted (IVW) method was utilized for the preliminary estimates, and multiple sensitivity analyses (including weighted median, Cochran's Q test, MR‐Egger, MR‐PRESSO, and leave‐one‐out analysis) were conducted to verify the robustness of the results. The MR analyses using the IVW method showed that genetically predicated PA was significantly associated with atrial fibrillation (OR = 1.046, 95% CI: 1.029–1.062, padj < 0.001), myocardial infarction (OR = 1.029, 95% CI: 1.005–1.053, padj = 0.027), heart failure (OR = 1.023, 95% CI: 1.004–1.042, padj = 0.027), any stroke (OR = 1.062, 95% CI: 1.031–1.095, padj < 0.001), any ischemic stroke (OR = 1.058, 95% CI: 1.022–1.095, padj = 0.004), and small vessel stroke (OR = 1.116, 95% CI: 1.041–1.196, padj = 0.004). Notably, PA also had a causal effect on adverse cardiac remodeling, including larger ventricular and atrial volumes, higher ventricular stroke volume, and reduced left atrial emptying fraction. Our findings support a causal role of PA in higher cardiovascular disease risk and adverse cardiac remodeling. Given the diagnostic delay and disease burden in PA, more attention should be paid to the screening and treatment of PA to reduce the incidence of cardiovascular outcomes. [ABSTRACT FROM AUTHOR]

Cardiometabolic disorders contribute to the global burden of cardiovascular diseases. Emerging sphingolipid metabolites like sphingosine‐1‐phosphate (S1P) and its receptors, S1PRs, present a dynamic signalling axis significantly impacting cardiac homeostasis. S1P's intricate mechanisms extend to its transportation in the bloodstream by two specific carriers: high‐density lipoprotein particles and albumin. This intricate transport system ensures the accessibility of S1P to distant target tissues, influencing several physiological processes critical for cardiovascular health. This review delves into the diverse functions of S1P and S1PRs in both physiological and pathophysiological conditions of the heart. Emphasis is placed on their diverse roles in modulating cardiac health, spanning from cardiac contractility, angiogenesis, inflammation, atherosclerosis and myocardial infarction. The intricate interplays involving S1P and its receptors are analysed concerning different cardiac cell types, shedding light on their respective roles in different heart diseases. We also review the therapeutic applications of targeting S1P/S1PRs in cardiac diseases, considering existing drugs like Fingolimod, as well as the prospects and challenges in developing novel therapies that selectively modulate S1PRs. [ABSTRACT FROM AUTHOR]

Background/Objectives: The impact of alcohol consumption and its restriction on clinical outcomes in patients undergoing percutaneous coronary intervention (PCI) remains elusive. We aimed to investigate the clinical outcomes in drinkers undergoing PCI. Methods: We included 77,409 patients who underwent PCI and a health check-up within one year of the PCI using a nationwide prospective database from the Korean National Health Insurance System. Primary outcomes were major adverse cardiovascular and cerebrovascular events (MACCE), a composite of all-cause mortality, myocardial infarction, coronary revascularization, and stroke. Patients were classified as non-drinkers, within-the-guideline (≤1 standard drink in women and ≤2 in men), and above-the-guideline drinkers based on drinking status at the first health check-up after PCI. Results: During a 4.0-year follow-up duration, MACCE incidence was 19.7% (n = 15,214) (4689 [6.1%] deaths, 1916 [2.5%] MI, 2033 [2.6%] strokes, and 10,086 [13.0%] revascularizations). Both within-the-guideline- (aHR [95%CI], 0.843 [0.773–0.919]) and above-the-guideline drinkers (0.829 [0.784–0.876]) had a lower MACCE risk than the non-drinkers. A characteristic J-curve relationship was observed between the frequency or body weight-adjusted alcohol consumption and MACCE risk, with the lowest risk in the once-per-week and a mild amount per body weight (≤0.33 g/kg/week) group. Drinking habits after PCI were associated with a lower risk of adverse cardiovascular outcomes; those who continued to drink before and after PCI had the lowest risk. Conclusions: Alcohol consumption was associated with a lower risk of adverse outcomes in patients undergoing PCI. Further studies with longer-term follow-up are warranted. [ABSTRACT FROM AUTHOR]

Dual antiplatelet therapy (DAPT), which is essential in AMI management, combines aspirin with a P2Y12 receptor antagonist. This study compared the effectiveness of potent P2Y12 inhibitors versus clopidogrel in AMI patients treated with percutaneous coronary intervention (PCI). Methods: 65,986 AMI patients included in a nationwide prospective registry who underwent PCI and received DAPT were studied. In total, 9,014 patients received potent P2Y12 inhibitors, and 56,074 received clopidogrel. This study focused on mortality, recurrent myocardial infarction, stroke, repeat revascularization, and major adverse cardiovascular events (MACE) over seven years. The analysis utilized unadjusted models and inverse probability of treatment weighting (IPTW) to compare prognosis, and decision curve analyses were constructed to aid clinical decision making. Results: Potent P2Y12 inhibitors significantly reduced mortality risk (unadjusted hazard ratio (HR): 0.58; IPTW HR: 0.68) and MACE (unadjusted HR: 0.66; IPTW HR: 0.78). Diabetic patients showed greater benefits (HR:0.45). In patients at high bleeding risk, the mortality rate was 13% (HR: 0.87, p = 0.08). For patients aged 75–79, the HR for mortality was 0.82, whereas for those aged >80 years, it was 0.79, indicating significant mortality risk reduction. Similar trends were observed for MACE. Conclusion: This study demonstrated that potent P2Y12 inhibitors are more effective than clopidogrel in reducing mortality and MACE in patients with AMI and underscored their potential role in improving outcomes across diverse patient subgroups. The trend was consistent even during the COVID-19 pandemic. These findings highlight the need for personalized DAPT strategies, particularly for high-bleeding-risk patients, and challenge current guidelines favoring clopidogrel use in older patients. [ABSTRACT FROM AUTHOR]

Background/Objectives: In recent decades, the number of patients with chronic cardiovascular diseases (CVDs) has increased, and CVD survivors are more likely to be old and frail and to have multiple comorbidities. A better understanding of geriatric conditions and their prevalence would help improve the management of older patients with CVDs. The main objective of this study is to estimate the association of myocardial infarction (MI) history with geriatric syndromes (GSs) in people 65 years of age and older. Methods: The cross-sectional study EVKALIPT included patients who were 65 years of age and older. All patients underwent a comprehensive geriatric assessment. The presence of MI history was assessed by medical records. Results: A total of 4295 participants were included. The prevalence of MI history was 12.6%. According to univariate regression analysis, MI history was associated with an increase in the odds of 12 GSs by 1.3–2.4 times. Multivariate regression analysis showed that male sex and four GSs (impairment in basic and instrumental activities of daily living, depression, falls) were independently associated with a history of MI, with the odds ratio ranging from 1.28 to 1.86. Conclusions: This study showed the association between MI history and GSs. [ABSTRACT FROM AUTHOR]

We examined the prospective associations of social isolation and loneliness with incident cardiovascular disease (CVD) among aging nonveteran and veteran women, and effect modification by veteran status. Participants with no history of myocardial infarction (MI), stroke, coronary heart disease (CHD), or coronary heart failure from the Women's Health Initiative Extension Study II self-reported social isolation, loneliness, health behaviors, health status, and veteran status. CVD and CVD subevents were physician adjudicated. Hazard ratios (HR) and 95% confidence intervals (CI) for the Interquartile Range (IQR) in social isolation (IQR = 1) and loneliness (IQR=.33) were calculated using Cox proportional hazard models adjusting for sociodemographic, health behavior, and health status characteristics. Veteran status was tested as an effect modifier. Among 52,442 women (Mean age = 79 ± 6.1; veterans n = 1023; 89.2% non-Hispanic White), 3579 major CVD events occurred over an average 5.8 follow-up years. Compared to nonveterans, veteran women reported higher levels of social isolation (p <.01) and loneliness (p <.01). The CVD HR was 1.07 (95% CI, 1.04–1.10) for the IQR in social isolation and 1.03 (95% CI, 1.10–1.06) for the IQR in loneliness. The HR for the IQR in both social isolation and loneliness was 1.10 (95% CI, 1.05–1.15). Social isolation was associated with CHD (HR = 1.12; 95% CI, 1.03–1.21). The CHD HR for the IQR in social isolation was 1.12 (95% CI, 1.03–1.21). Associations did not differ by veteran status (all p-interactions > 0.08). Findings suggest that the adverse associations of social isolation and loneliness with CVD are similar among veteran and nonveteran women. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) is a critical global health issue and a leading cause of heart failure. Indeed, while neonatal mammals can regenerate cardiac tissue mainly through cardiomyocyte proliferation, this ability is lost shortly after birth, resulting in the adult heart's inability to regenerate after injury effectively. In adult mammals, the adverse cardiac remodelling, which compensates for the loss of cardiac cells, impairs cardiac function due to the non-contractile nature of fibrotic tissue. Moreover, the neovascularisation after MI is inadequate to restore blood flow to the infarcted myocardium. This review aims to synthesise the most recent insights into the molecular and cellular players involved in endogenous myocardial and vascular regeneration, facilitating the identification of mechanisms that could be targeted to trigger cardiac regeneration, reduce fibrosis, and improve functional recovery post-MI. Reprogramming adult cardiomyocytes to regain their proliferative potential, along with the modulation of target cells responsible for neovascularisation, represents promising therapeutic strategies. An updated overview of endogenous mechanisms that regulate both myocardial and coronary vasculature regeneration—including stem and progenitor cells, growth factors, cell cycle regulators, and key signalling pathways—could help identify new critical intervention points for therapeutic applications. [ABSTRACT FROM AUTHOR]

The structure of aspirated coronary thrombus in ST-segment elevation myocardial infarction (STEMI) is still being studied. Our aims were to characterize coronary thrombi of different ages, focusing on the appearance of activated protein C (APC/PC) and its relation to the elements of neutrophil extracellular traps (NETs), and the factors closely related to fibrin as factor XIII (FXIII) and α2 plasmin inhibitor (α2-PI). The thrombi of n = 24 male patients with atherosclerotic coronary plaque rupture related to native coronary artery occlusion were selected for histopathology analysis. Thrombus age was distinguished as fresh, lytic, and organized, and then analyzed by immunofluorescent staining and confocal microscopy. FXIII was present at a high level and showed a high degree of co-localization with fibrin in all stages of thrombus evolution. The amount of α2-PI was low in the fresh thrombi, which increased significantly to the lytic phase. It was evenly distributed and consistently associated with fibrin. APC/PC appeared in the fresh thrombus and remained constant during its evolution. The presence of NET marker and CD66b was most dominant in the lytic phase. APC/PC co-localization with the elements of NET formation shows its role in NET degradation. These observations suggest the importance of searching for further targeted therapeutic strategies in STEMI patients. [ABSTRACT FROM AUTHOR]

Background: The risk of life‐threatening major cardiovascular outcomes among patients with bullous pemphigoid (BP) is inconsistent in the current literature. Objective: To evaluate the risk and prognostic outcomes of myocardial infarction (MI), cerebrovascular accident (CVA), peripheral vascular disease (PVD) and pulmonary embolism (PE) in patients with BP. We additionally aimed to explore the influence of different therapeutic approaches on the risk of these outcomes. Methods: A population‐based retrospective cohort study was conducted to compare BP patients (n = 3924) with age‐, gender‐ and ethnicity‐matched control subjects (n = 19,280) with regard to incident cases of MI, CVA, PVD and PE. Adjusted hazard ratio (HR) and 95% confidence intervals (CI) were estimated by multivariate Cox regression analysis. Data were retrieved from Clalit Health Services' computerized database. Results: Relative to their matched controls, patients with BP were at an elevated risk of MI (fully‐adjusted HR: 1.44; 95% CI: 1.14–1.81; p = 0.002), CVA (fully‐adjusted HR: 1.24; 95% CI: 1.06–1.45; p = 0.007), PVD (fully‐adjusted HR: 1.60; 95% CI: 1.27–2.03; p = 0.003) and PE (fully‐adjusted HR: 1.72; 95% CI: 1.28–2.32; p < 0.008). Patients with BP experienced heightened risk of all‐cause mortality in the presence of comorbid MI (fully‐adjusted HR: 1.61; 95% CI: 1.44–1.81; p < 0.001), CVA (fully‐adjusted HR: 1.70; 95% CI: 1.52–1.89; p < 0.001), PVD (fully‐adjusted HR: 1.38; 95% CI: 1.20–1.58; p < 0.001) and PE (fully‐adjusted HR: 1.44; 95% CI: 1.10–1.88; p = 0.007). The therapeutic approach utilized to manage BP did not significantly influence the risk of cardiovascular outcomes. Conclusions: BP is associated with an elevated risk of MI, CVA, PVD, PE and cardiovascular mortality. Primary, secondary and tertiary cardiovascular prevention measures should be implemented among patients with BP. [ABSTRACT FROM AUTHOR]

The document discusses the association between high red cell mass (RCM) and high plasma volume with thrombotic risk in polycythemia vera (PV) patients. The study included 211 PV patients from Serbia and Croatia and found that patients with both high RCM and high plasma volume had the highest risk of thrombotic events. The findings suggest that RCM and plasma volume measurements may be important for prognostic purposes in PV, highlighting the need for further research and validation of these results in larger datasets and different populations. [Extracted from the article]

Introduction: Chronic myeloid leukemia (CML) is a hematological malignancy with an excellent prognostic outcome. After the advancements in CML treatment and the introduction of different tyrosine kinase inhibitors (TKIs), the life expectancy of CML patients has become equivalent to that of the general population. As a result, coronary artery disease is anticipated to be the leading cause of death among CML patients. Moreover, TKI use is associated with a risk of endothelial dysfunction, thrombosis, and cardiovascular events, including myocardial infarction. In this study, we compare the outcomes of percutaneous coronary intervention (PCI) in patients with CML to their matched non-CML counterparts. Method: This is a retrospective cohort study using the Nationwide Readmission Database from January 2016 to December 2020. Adults with or without CML hospitalized for acute myocardial infarction and underwent PCI were included. The patients were identified using ICD-10 codes. The primary outcomes were in-hospital mortality and 30-day readmission rates. The secondary outcomes were PCI complications rates. Results: Out of 2,727,619 patients with myocardial infarction, 2,124 CML patients were identified. A total of 888 CML patients underwent PCI. CML patients were significantly older (mean age: 68.34 ± 11.14 vs. 64.40 ± 12.61 years, p < 0.001) than non-CML patients without a difference in sex distribution. Hypertension (85.45% vs. 78.64%), diabetes (45.48% vs. 37.29), stroke (11.84% vs. 7.78) at baseline were significantly higher in the CML group. Prior myocardial infarction events (20.51% vs. 15.17%) and prior PCI procedure (24.47% vs. 16.89%) were significantly higher in the CML group. CML patients had a significantly longer hospital stay (4.66 ± 4.40 vs. 3.75 ± 4.62 days, p = 0.001). The primary outcomes did not differ between the comparison groups. The risk of post-PCI complications did not differ between the comparison groups in the propensity matched analysis except for coronary artery dissection (odds ratio [OR]: 0.10; 95% confidence interval [CI]: 0.02–0.65, p = 0.016) and ischemic stroke (OR: 0.35; 95% CI: 0.14–0.93, p = 0.034) which were lower in the CML group. Conclusion: This analysis showed no statistically significant difference in mortality, 30-day readmission, and post PCI complications rates between CML and non-CML patients. However, interestingly, CML patients may experience lower coronary artery dissection and ischemic stroke events than those without CML diagnosis. [ABSTRACT FROM AUTHOR]

The management of cardiogenic shock is an ongoing challenge. Despite all efforts and tremendous use of resources, mortality remains high. Whilst reversing the underlying cause, restoring/maintaining organ perfusion and function are cornerstones of management. The presence of comorbidities and preexisting organ dysfunction increases management complexity, aiming to integrate the needs of vital organs in each individual patient. This review provides a comprehensive overview of contemporary literature regarding the definition and classification of cardiogenic shock, its pathophysiology, diagnosis, laboratory evaluation, and monitoring. Further, we distill the latest evidence in pharmacologic therapy and the use of mechanical circulatory support including recently published randomized-controlled trials as well as future directions of research, integrating this within an international group of authors to provide a global perspective. Finally, we explore the need for individualization, especially in the face of neutral randomized trials which may be related to a dilution of a potential benefit of an intervention (i.e., average effect) in this heterogeneous clinical syndrome, including the use of novel biomarkers, artificial intelligence, and machine learning approaches to identify specific endotypes of cardiogenic shock (i.e., subclasses with distinct underlying biological/molecular mechanisms) to support a more personalized medicine beyond the syndromic approach of cardiogenic shock. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cell (MSC) therapy aids cardiac repair and regeneration, but the low rate of MSC survival and engulfment in the infarcted heart remains a major obstacle for routine clinical application. Here, an injectable suspension of human acellular amniotic membrane (HAAM) that may serve as synergistic cell delivery vehicle for the treatment of myocardial infarction (MI) by improving MSC homing and survival is developed. The results demonstrate that compared with MSC transplantation alone, HAAM‐loaded MSCs have higher survival and engraftment rates in infarcted tissue, alleviated hypoxia‐induced myocardial damage, achieved higher improvements in cardiac function, promoted angiogenesis, and reduced myocardial fibrosis. In addition, HAAM‐loaded MSCs increase N‐cadherin levels and thereby enhance the efficacy of MSCs in treating MI. This study provides a new approach for MSC‐based cardiac repair and regeneration. [ABSTRACT FROM AUTHOR]

Sudden cardiac arrest (SCA) represents a major cause of premature mortality globally, with enormous impact and financial cost to victims, families, and communities. SCA prevention should be considered a health priority in Australia. National Cardiac Arrest Summits were held in June 2022 and March 2023, with inclusion from multi-faceted endeavours related to SCA prevention. It was agreed to establish a multidisciplinary Australian Sudden Cardiac Arrest Alliance (AuSCAA) working group charged with developing a national unified strategy, with clear and measurable quality indicators and standardised outcome measures, to amplify the goal of SCA prevention throughout Australia. A multi-faceted prevention strategy will include i) endeavours to progress community awareness, ii) improved fundamental mechanistic understanding, iii) implementation of best-practice resuscitation strategies for all demographics and locations, iv) secondary risk assessment directed to family members, and v) development of (near) real-time registry of cardiac arrest cases to inform areas of need and effectiveness of interventions. Together, we can and should reduce the impact of SCA in Australia. [ABSTRACT FROM AUTHOR]

This meta-analysis aimed to evaluate the effects of intracoronary (IC) low-dose tirofiban versus intravenous (IV) administration on clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). All published randomised controlled trials (RCTs) comparing the effects of IC low-dose tirofiban (a bolus of ≤10 ug/kg) versus IV administration in patients with STEMI were identified by searching PubMed, EMBASE, Cochrane Library, and ISI Web of Science from inception to June 2023, with no language restriction. The risk ratio (RR) with 95% confidence intervals (CI) and the weighted mean difference (WMD) with 95% CI were calculated. Eleven RCTs involving 1,802 patients were included. Compared with the IV group, IC low-dose tirofiban was associated with improved major adverse cardiac events rate (RR 0.595, 95% CI 0.442–0.802; p=0.001), left ventricular ejection fraction (WMD 1.982, 95% CI 0.565–3.398; p=0.006), thrombolysis in myocardial infarction (TIMI) flow grade (RR 1.065, 95% CI 1.004–1.131; p=0.037), and TIMI myocardial perfusion grade (RR 1.194, 95% CI 1.001–1.425; p=0.049). The two groups had no significant difference in bleeding events (RR 0.952, 95% CI 0.709–1.279; p=0.745). Intracoronary low-dose tirofiban administration may be a safe and effective alternative to IV administration in STEMI patients. [ABSTRACT FROM AUTHOR]

Introduction: Atrial fibrillation (AF) is the most common sustained arrhythmia, and catheter ablation (CA) is a primary therapeutic option. However, the 30‐day all‐cause mortality risk associated with CA for AF may be underestimated due to selection bias. Our study aimed to assess 30‐day mortality in an unselected cohort of patients. Methods: Data from the National Health Fund‐Poland covered over 99% of nationwide radiofrequency ablation (RF) or cryoballoon ablation for AF, with 100% recorded deaths. The study included consecutive CA procedures in adult patients between 2012 and 2019. Thirty‐day mortality rates were calculated for each age group. Results: A total of 31 214 CAs for AF were performed on 26 767 patients (34.8% female). Forty‐four percent of patients had hypertension, 31.2% had coronary artery disease, 14.4% had heart failure, 11% had diabetes mellitus, 5.6% had malignant neoplasms, 2.7% had a previous myocardial infarction, 2.5% had a previous stroke, and 2.2% had kidney disease. Thirty‐two deaths (0.1%) occurred within 30 days, with the highest mortality in the oldest age group (>80 years). Statistical analysis revealed higher incidences of kidney disease (p < 0.001) and heart failure (p = 0.001) in patients who died within 30 days. Mortality risk did not significantly differ between cryoballoon and RF ablation, as well as first and subsequent ablation for AF. The risk of death within 7 days postablation for AF was 1 in 2750 procedures, while the risk of death on the same day postablation was 1 in 6250 procedures. Conclusions: The 30‐day mortality rate in a large, unselected AF ablation cohort, covering 99% of procedures in the country, is low except for the oldest patients. This factor should be taken into consideration when offering CA for AF. [ABSTRACT FROM AUTHOR]

Randomized trials estimate the average treatment effect within individuals who are eligible, invited, and agree to enroll. However, decision-makers often require evidence that extends beyond the trial's enrolled population to inform policy or actions for their specific target population. Each decision-maker has distinct target populations, the composition of which may not often align with that of the trial population. As researchers, we should identify a decision-maker for whom we aim to generate evidence early in the research process. We can then specify a target population of their interest and determine if a policy or action can be informed using results from a trial alone, or if additional complementary real-world data and analysis are required. In this commentary, we outline 5 key groupings of decision-makers: policymakers, payers, purchasers, providers, and patients. We then specify relevant target populations for decision-makers interested in the effectiveness of beta-blockers after a myocardial infarction with preserved ejection fraction. Finally, we summarize the scenarios in which results from a randomized trial may or may not apply to these target populations and suggest relevant analytic approaches that can generate evidence to better align with a decision-maker's needs. This article is part of a Special Collection on Pharmacoepidemiology. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction is the most common cardiovascular disease and 85% of cardiovascular disease-related deaths are associated with it. The variation in the cardiac troponin concentration is considered as the most significant judge index for acute myocardial infarction diagnosis. Here, a comprehensive insights is given about the impedimetric methods as powerful electrochemical biosensing platforms for cardiac troponin evaluation. Focusing on nano materials, various impedimetric techniques including faradaic and non-faradaic techniques and different transducer modification techniques are addressed. The steps taken by each of the studied platforms to solve the existing problems are discussed and their advantages and drawbacks are highlighted. A glance at the provided table is given a mind into the features of each impedimetric sensors and their comparison are provided. [ABSTRACT FROM AUTHOR]

Troponin I as a particular and major biomarker of cardiac failure is released to blood demonstrating hurt of myocardial cells. Unfortunately, troponin I detection in the first hours of acute myocardial infarction usually faces with most negligence. Therefore, developments of point of care devices such as lateral flow strips are highly required for timely diagnosis and prognosis. Lateral flow assays are low-cost paper-based detection platforms relying on specific diagnostic agents such as aptamers and antibodies for a rapid, selective, quantitative and semi-quantitative detection of the analyte in a complex mixture. Moreover, lateral flow assay devices are portable, and their simplicity of use eliminates the need for experts or any complicated equipment to operate and interpret the test results. Additionally, by coupling the lateral flow assay technology with nanotechnology, for labeling and signal amplification, many breakthroughs in the field of diagnostics have been achieved. The present study reviews the use of lateral flow assays in early stage, quantitative, and sensitive detection of cardiac troponin I and mainly focuses on the structure of each type of developed lateral flow assays. Finally, this review summarized the improvements, detection time, and limit of detection of each study as well as the advantages and disadvantages. [ABSTRACT FROM AUTHOR]

Purpose: Generating polar map (PM) from [68Ga]Ga-DOTA-FAPI-04 PET images is challenging and inaccurate using existing automatic methods that rely on the myocardial anatomical integrity in PET images. This study aims to enhance the accuracy of PM generated from [68Ga]Ga-DOTA-FAPI-04 PET images and explore the potential value of PM in detecting reactive fibrosis after myocardial infarction and assessing its relationship with cardiac function. Methods: We proposed a deep-learning-based method that fuses multi-modality images to compensate for the cardiac structural information lost in [68Ga]Ga-DOTA-FAPI-04 PET images and accurately generated PMs. We collected 133 pairs of [68Ga]Ga-DOTA-FAPI-04 PET/MR images from 87 ST-segment elevated myocardial infarction patients for training and evaluation purposes. Twenty-six patients were selected for longitudinal analysis, further examining the clinical value of PM-related imaging parameters. Results: The quantitative comparison demonstrated that our method was comparable with the manual method and surpassed the commercially available software-PMOD in terms of accuracy in generating PMs for [68Ga]Ga-DOTA-FAPI-04 PET images. Clinical analysis revealed the effectiveness of [68Ga]Ga-DOTA-FAPI-04 PET PM in detecting reactive myocardial fibrosis. Significant correlations were demonstrated between the difference of baseline PM FAPI% and PM LGE%, and the change in cardiac function parameters (all p < 0.001), including LVESV% (r = 0.697), LVEDV% (r = 0.621) and LVEF% (r = -0.607). Conclusion: The [68Ga]Ga-DOTA-FAPI-04 PET PMs generated by our method are comparable to manually generated and sufficient for clinical use. The PMs generated by our method have potential value in detecting reactive fibrosis after myocardial infarction and were associated with cardiac function, suggesting the possibility of enhancing clinical diagnostic practices. Trial registration: ClinicalTrials.gov (NCT04723953). Registered 26 January 2021. [ABSTRACT FROM AUTHOR]