Outcomes In Myocardial Infarction Patients Research Articles

Advancing Myocardial Infarction Treatment: Harnessing Multi-Layered Recellularized Cardiac Patches with Fetal Myocardial Scaffolds and Acellular Amniotic Membrane.

Myocardial infarction (MI) is a leading cause of irreversible functional cardiac tissue loss, requiring novel regenerative strategies. This study assessed the potential therapeutic efficacy of recellularized cardiac patches, incorporating fetal myocardial scaffolds with rat fetal cardiomyocytes and acellular human amniotic membrane, in adult Wistar rat models of MI. Decellularized myocardial tissue was obtained from 14 to 16 week-old human fetuses that had been aborted. Chemical detergents (0.1% EDTA and 0.2% sodium dodecyl sulfate) were used to prepare the fetal extracellular matrix (ECM), which was characterized for bio-scaffold microstructure and biocompatibility via scanning electron microscopy (SEM) and MTT assay, respectively. Neonatal cardiomyocytes were extracted from the ventricles of one-day-old Wistar rats' littermates and characterized through immunostaining against Connexin-43 and α-smooth muscle actin. The isolated cells were seeded onto decellularized tissues and covered with decellularized amniotic membrane. Sixteen healthy adult Wistar rats were systematically allocated to control and MI groups. MI was induced via arterial ligation. Fourteen days post-operation, the MI group was received the engineered patches. Following a two-week post-implantation period, the animals were euthanized, and the hearts were harvested for the graft evaluation. Histological analysis, DAPI staining, and ultra-structural examination corroborated the successful depletion of cellular elements, while maintaining the integrity of the fetal ECM and architecture. Subsequent histological and immunohistochemichal (IHC) evaluations confirmed effective cardiomyocyte seeding on the scaffolds. The application of these engineered patches in MI models resulted in increased angiogenesis, reduced fibrosis, and restricted scar tissue formation, with the implanted cardiomyocytes remaining viable at graft sites, indicating prospective in vivo cell viability. This study suggests that multi-layered recellularized cardiac patches are a promising surgical intervention for myocardial infarction, showcasing significant potential by promoting angiogenesis, mitigating fibrosis, and minimizing scar tissue formation in MI models. These features are pivotal for enhancing the therapeutic outcomes in MI patients, focusing on the restoration of the myocardial structure and function post-infarction.

Vitamin D deficiency and its impact on outcomes in myocardial infarction patients: a prospective observational study

Objectives: Vitamin D deficiency has been linked to cardiovascular diseases, but its impact on outcomes in myocardial infarction (MI) patients remains unclear. This study investigated the relationship between serum vitamin D levels and short-term and medium-term outcomes in patients with myocardial infarction. Ischemic heart diseases (IHD) are the most common cause of death in the world. Identifying risk factors and predictors can play a critical role in identifying high-risk people in screenings, identifying high-risk patients during admission to the hospital, and adjusting these risk factors in patients to improve prognosis. Methods: This prospective observational study was conducted on 212 patients diagnosed with myocardial infarction at Seyed al-Shohada Hospital in Urmia, Iran. Having been admitted, the patients had their serum vitamin D levels measured using the same blood sample for routine tests. Levels of vitamin D were categorized as normal (>30 ng/ml), insufficient (21-29 ng/ml), or deficient (<20 ng/ml). The patient's files provided the demographic, clinical, and biomedical information, echocardiography, and angiography data. The patients were followed for at least six months post-MI, with a maximum follow-up of 11 months. Follow-up occurred through monthly phone calls and outpatient clinic visits as needed. Primary outcomes included in-hospital complications (such as death, significant bleeding, acute pulmonary edema, cardiogenic shock, and arrhythmias), cardiac readmissions, and mortality. Logistic regression and Cox regression analyses were used to examine the connection between outcome variables and vitamin D levels, adjusting for potential confounders including age, gender, blood pressure, diabetes, blood lipids, creatinine, disease severity (SYNTAX score*), and left ventricular ejection fraction. The mean serum level of vitamin D in patients on admission was 33. 62 ng/dL. The average number of hospitalization days was 4.8 days, and the rate of re-hospitalization was 26.6% in the six-month follow-up and 30.3% in the 9-month follow-up. The hospital mortality rate was equal to 1.4%, and the mortality rate at the end of the follow-up period was equal to 8.3%. The most common complication during hospitalization among the patients was ventricular tachycardia. However, in follow-up, re-hospitalization due to previous issues was the most common complication. Results: The mean serum vitamin D level was 33. 62 ng/ml,with 52.8% of patients having insufficient or deficient levels. The most common in-hospital complication was ventricular tachycardia (11.5%). Vitamin D deficiency was not significantly associated with in-hospital complications. However, during the follow-up period, vitamin D deficiency was significantly related to increased risk of readmission to hospital (HR: 6.984, 95% CI: 3.500-13.936, p<0.001). The 6-month readmission rate was 26.6%, increasing to 30.3% at 9 months. Vitamin D deficiency was also associated with increased cardiac mortality (HR: 12.936, 95% CI: 1.494- 112.016, p=0.020) during follow-up. The 9-month mortality rate was 8.3%. Other factors contributing to cardiac mortality included disease severity (SYNTAX score) and female gender. Conclusions: While vitamin D deficiency did not impact short-term complications, it was associated with increased risk of hospitalreadmission and mortality in MI patients during medium-term follow-up. These findings suggest that vitamin D status can significantly impact long-term outcomes for MI patients

Survival outcomes correlate with the level of cell-free circulating DNA in ST-elevation myocardial infarction.

Myocardial infarction (MI) can lead to higher cellular damage, making cell-free DNA (cfDNA) a potential biomarker for assessing disease severity. The aim of this study is to evaluate survival predictions using cfDNA measurements and assess its correlation with MI. A direct fluorescence assay was employed to measure cfDNA content in the blood samples of participants. The inclusion criteria included patients who gave informed consent, suffering from ST-elevation myocardial infraction (STEMI) based on established diagnostic criteria (joint ESC/ACC guidelines), between the age of 18 and 80 years old, and had elevated troponin biomarker levels. The study included 150 patients diagnosed with STEMI and 50 healthy volunteers as controls. Serial monitoring of patients was conducted to track their postdisease status. The rate of change of cfDNA was calculated and daily measurements for 7 days were recorded. Mean levels of cfDNA were found to be 5.93 times higher in patients with STEMI compared to healthy controls, providing clear evidence of a clinical correlation between cfDNA and STEMI. Patients were further categorized based on their survival status within a 90-day period. The study observed a strong predictive relationship between the rate of change of cfDNA during daily measurements and survival outcomes. To assess its predictive capability, a receiver operating characteristics (ROC) curve analysis was performed. The ROC analysis identified an optimal cutoff value of 2.50 for cfDNA, with a sensitivity of 81.5% and specificity of 74.0% in predicting disease outcomes. This study demonstrates a robust association between cfDNA and STEMI, indicating that cfDNA levels can be a valuable early prognostic factor for patients. Serial measurements of cfDNA during early disease onset hold promise as an effective approach for predicting survival outcomes in MI patients.

Impact of residual coronary lesions on outcomes of myocardial infarction patients with multi-vessel disease

BackgroundThe residual burden of coronary artery disease (CAD) after percutaneous coronary intervention (PCI) drew a growing interest. The residual SYNTAX Score (rSS) was a strong prognostic factor of adverse events and all-cause mortality in patients who underwent PCI. In addition, the SYNTAX Revascularization Index (SRI), a derivative of rSS, was used to figure out the treated proportion of CAD and could be used as a prognostic utility in PCI for patients with multi-vessel disease (MVD).PurposeWe aimed at the assessment of the use of rSS and the SRI as predictors of in-hospital outcomes and up to two-year cumulative follow-up outcomes in patients with MVD who had PCI for the treatment of ST-Elevation Myocardial Infarction (STEMI) or Non-STEMI (NSTEMI).MethodsWe recruited 149 patients who had either STEMI or NSTEMI while having MVD and received treatment with PCI. We divided them into tertiles based on their rSS and SRI values. We calculated baseline SYNTAX Score (bSS) and rSS using the latest version of the calculator on the internet, and we used both scores to calculate SRI. The study end-points were In-hospital composite Major Adverse Cardiovascular Events (MACE) and its components, in-hospital death, and follow-up cumulative MACE up to 2 years.ResultsNeither rSS nor SRI were significant predictors of in-hospital adverse events, while female sex, hypertension, and left ventricular ejection fraction were independent predictors of in-hospital MACE. At the two-year follow-up, Kaplan-Meyer analysis showed a significantly increased incidence of MACE within the third rSS tertile (rSS > 12) compared to other tertiles (log rank p = 0.03). At the same time, there was no significant difference between the three SRI tertiles. Unlike SRI, rSS was a significant predictor of cumulative MACE on univariate Cox regression (HR = 1.037, p < 0.001). On multivariate Cox regression, rSS was a significant independent predictor of two-year cumulative MACE (HR = 1.038, p = 0.0025) along with female sex, hypertension, and left ventricular ejection fraction. We also noted that all patients with complete revascularization survived well throughout the entire follow-up period.ConclusionsNeither rSS nor SRI could be good predictors of in-hospital MACE, while the rSS was a good predictor of MACE at two-year follow-up. Patients with rSS values > 12 had a significantly higher incidence of cumulative MACE after 2 years. The best prognosis was achieved with complete revascularization.

Effect of Intensive Glycemic Control on Myocardial Infarction Outcome in Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis.

The effect of intensive glucose-lowering treatment on the risk of cardiovascular events in type 2 diabetes remains uncertain, especially the effect on the occurrence of myocardial infarction in patients with type 2 diabetes is still unclear. The purpose of this study was to conduct a systematic review and meta-analysis of relevant RCTs. We performed a systematic review of randomized clinical trials (RCTS) and observational studies relevant to this study question. We searched the PubMed and Cochrane databases until June 2022. We included data on 14 RCTs and 144,334 patients, all of whom had type 2 diabetes. When all studies were considered, intensive glucose-lowering treatment significantly reduced the incidence of MI compared with conventional therapy and the total OR value is 0.90 (CI 0.84, 0.97; P = 0.004) when considering all the studies. When the target value of intensive glucose-lowering treatment was considered as HbA1c decrease of more than 0.5%, there was no significant protective effect on MI, the total OR value is 0.88 (CI 0.81, 0.96; P = 0.003). When considering all available RCTS, the intensive glucose-lowering treatment group had a protective effect for MACE compared to the conventional treatment group, and the total OR value is 0.92 (CI 0.88, 0.96; P < 0.00001). In the available RCTs, for the patients with a history of prior CAD, the total OR value is 0.94 (CI 0.89, 0.99; P = 0.002). And there was no difference in the incidence of hypoglycemic events between the intensive and conservative treatment groups. Our data support the positive protective effect of glucose-lowering therapy on MI in patients with T2DM, but there is no significant effect of intensive glucose-lowering. In addition, we found no greater protective effect of enhanced glucose control in the HbA1c reduction of more than 0.5%, and no difference in the incidence of adverse events compared with the HbA1c reduction of less than 0.5%.

Invasive Management and In-Hospital Outcomes of Myocardial Infarction Patients in United States Safety-Net Hospitals

AimSafety-net hospitals (SNHs) look after a higher proportion of uninsured patients and are often located in deprived areas. This study aimed to determine whether there are differences in the clinical characteristics, treatments and outcomes of patients presenting with acute myocardial infarction (AMI) in SNHs versus non-SNHs (N-SNHs). MethodsAll hospitalizations with a principal diagnosis of AMI in the United States' National Inpatient Sample between 2016 and 2019 were stratified by safety-net hospital status. Multivariable logistic regression with adjusted odds ratios (aOR) and 95 % confidence intervals (95 % CI) was conducted to investigate invasive management and clinical outcomes. ResultsA total of 2,544,009 weighted discharge records were analyzed, including 601,719 records from SNHs (23.7 %). Compared with N-SNHs, SNH AMI patients were younger (median 66 years vs. 67 years, p < 0.001), and had a higher proportion in the lowest quartile of median household income (37.3 % vs. 28.5 %, p < 0.001). Patients from SNHs were less likely to receive coronary angiography (aOR 0.92, 95 % CI 0.91–0.93, p < 0.001), percutaneous coronary intervention (aOR 0.94, 95 % CI 0.93–0.95, p < 0.001), and coronary artery bypass grafting (aOR 0.93, 95 % CI 0.92–0.94, p < 0.001). In addition, they had increased all-cause mortality (aOR 1.11, 95 % CI 1.09–1.12, p < 0.001), major adverse cardiovascular/cerebrovascular events (composite of mortality, stroke and reinfarction) (aOR 1.11, 95 % CI 1.09–1.12, p < 0.001), and stroke (aOR 1.11, 95 % CI 1.08–1.14, p < 0.001), while there was no difference in major bleeding (aOR 1.02, 95 % CI 1.00–1.04, p = 0.107). ConclusionAmong AMI patients, treatment in SNHs was associated with lower utilization of coronary angiography and revascularization and worse clinical outcomes.

Role of bilirubin in the prognosis of coronary artery disease and its relationship with cardiovascular risk factors: a meta-analysis

BackgroundBilirubin is a heme catabolism product with antioxidant, anti-inflammatory, and anti-apoptotic properties and is implicated in the prognosis of several diseases. This study evaluates the prognostic role of bilirubin in coronary artery disease (CAD) patients.MethodsAfter identifying studies from the literature, meta-analyses were performed to achieve a) overall estimates of serum total bilirubin levels in patients with myocardial infarction (MI), non-MI CAD and healthy individuals; b) odds ratios (OR) of adverse outcomes between higher and lower total bilirubin levels; c) standardized mean difference (SMD) in total bilirubin levels in patients with high vs low CAD severity; and d) correlation between disease severity and total bilirubin. Metaregression analyses were performed to examine the relationship between cardiovascular risk factors and increasing quantiles of total bilirubin levels.ResultsForty-three studies were identified. Pooled serum total bilirubin levels were 0.72 mg/dl [95% confidence interval (CI): 0.60, 0.83] in MI patients; 0.65 mg/dl [95% CI: 0.60, 0.69] in non-MI CAD patients; and 0.66 mg/dl [95% CI: 0.56, 0.75] in healthy individuals. Higher total bilirubin levels were associated with greater odds of adverse outcomes in MI patients (OR: 1.08 [95% CI: 0.99, 1.18]) but lower odds in non-MI CAD patients (OR: 0.80 [95%CI: 0.73, 0.88]). Compared to non-severe cases, total bilirubin levels were higher in patients with severe MI (SMD 0.96 [95% CI: − 0.10, 2.01]; p = 0.074) but were lower in severe non-MI CAD patients (SMD − 0.30 [95%CI: − 0.56, − 0.03]; p = 0.02). Total bilirubin levels correlated positively with MI severity (r = 0.41 [95% CI: 0.24, 0.59]; p < 0.01) but correlated negatively with non-MI CAD severity (r = − 0.17 [95% CI: − 0.48, 0.14]; p = 0.28). Female sex was inversely associated with increasing quantiles of bilirubin (meta-regression coefficient: − 8.164 [− 14.531, − 1.769]; p = 0.016) in MI patients.ConclusionPrognostic role of bilirubin for CAD appears complicated, as different odds are observed for MI and non-MI CAD patients which weakens the case of causal involvement of bilirubin in CAD etiology or prognosis.

Impact of residual coronary lesions on outcomes of myocardial infarction patients with multi-vessel disease

Abstract Background Interest grew in residual disease burden after percutaneous coronary intervention (PCI). The residual SYNTAX score (rSS) is a strong prognostic factor of coronary events and all-cause death in patients who underwent PCI. Its derivative, the SYNTAX Revascularisation Index (SRI), has been used in determining the proportion of coronary artery disease (CAD) that has been treated and has been shown to have prognostic utility in PCI for patients with multi-vessel disease (MVD). Purpose We sought to assess the use of the rSS and the SRI as predictors for in-hospital outcomes and up to two-year follow-up outcomes in patients with MVD who underwent PCI in the setting of ST-Elevation Myocardial Infarction (STEMI) or Non-STEMI (NSTEMI). Methods We recruited 149 patients with either STEMI or NSTEMI in the setting of MVD who underwent PCI. We divided them into tertiles, based on their rSS and SRI values, respectively. We calculated bSS and rSS using the latest version of the web-based calculator, and from these scores we calculated SRI. The endpoints were: In-hospital composite MACE and its components, in-hospital mortality, follow-up MACE, and follow-up all-cause mortality up to 2-years. Results RSS and SRI were not significant predictors of in-hospital death or MACE, while hypertension, ST-segment resolution, LVEF, and significant left main coronary artery (LMCA) lesions were independent predictors of in-hospital MACE. At two-year follow-up, Kaplan-Meier analysis showed significantly increased incidence of death and MACE within the third rSS tertile (rSS &amp;gt;12) compared to the other tertiles (log rank p&amp;lt;0.001), while there was no significant difference between the three SRI tertiles. RSS and SRI were predictors of death and MACE on univariate Cox regression analysis. On multivariate Cox regression, rSS was an independent predictor for MACE (HR=1.0696, 95% CI: 1.0147–1.1275, p=0.0123) and all-cause mortality (HR=1.1114, 95% CI: 1.0430–1.1842, p=0.0011). Of notice, all patients with complete revascularisation survived throughout the entire follow-up period. Conclusions The rSS and SRI were poor predictors of in-hospital death and MACE, while they were good predictors of death and MACE at two-year follow-up, with better overall performance for rSS in comparison to SRI. Patients with rSS values &amp;gt;12 showed significantly higher incidence of MACE and all-cause mortality at two years. The best prognosis was achieved with complete revascularisation. Funding Acknowledgement Type of funding sources: None.

Invasive Management and In-Hospital Outcomes of Myocardial Infarction Patients in Rural Versus Urban Hospitals in the United States

ObjectivesThe variation in the management and outcome of acute myocardial infarction (AMI) between rural and urban settings has been previously recognized, but there has previously been no nationwide data reported that is inclusive of the whole adult population. MethodsAll discharge records between 2004 and 2018 with AMI diagnosis were extracted from the National Inpatient Sample (NIS) database and stratified by hospital location. The primary outcome was in-hospital mortality, and secondary outcomes included (a) major adverse cardiovascular and cerebrovascular events (MACCE), (b) major bleeding, (c) acute ischemic stroke, the utilization of invasive management in the form of (d) coronary angiography (CA), and (e) percutaneous coronary intervention (PCI). The adjusted odds ratios (aOR) and 95 % confidence interval (95 % CI) were determined using multivariable logistic regression. Results9,728,878 records with AMI were identified, of which 1,011,637 (10.4 %) discharges were from rural hospitals. Rural patients were older (median of 71 years vs. 67 years, p < 0.001) and had lower prevalence of the highest risk presentations of AMI than their urban counterparts. After multivariable adjustment, patients from rural hospitals had increased aOR of all-cause mortality (aOR 1.15 95 % CI 1.13–1.16) and MACCE (aOR 1.04 95 % CI 1.04–1.05), as well as the decreased aOR of coronary angiography (aOR 0.29, 95 % CI 0.29–0.29, p < 0.001) and PCI (aOR 0.40, 95 % CI 0.39–0.40, p < 0.001), compared to their urban counterparts. ConclusionBetween 2004 and 2018, the risk of in-hospital mortality and MACCE in AMI patients was significantly higher in rural hospitals, with considerably lower utilization of invasive angiography and revascularization.

Impact of diabetes mellitus on outcomes in patients with myocardial infarction according to varying degrees of left ventricular systolic dysfunction.

Diabetes mellitus (DM) is known to contribute to unfavorable short- and long-term outcomes in patients with myocardial infarction (MI). Particularly poor outcomes are associated with left ventricular systolic dysfunction after an MI. Our study aimed to compare the short- and long-term outcomes of MI in patients with DM and varying degrees of left ventricular systolic dysfunction with the corresponding outcomes in a non-diabetic control group. This analysis focused on patients with MI registered in the Polish National Registry of Acute Coronary Syndrome between 2009 and 2011. For this analysis, diabetic patients were additionally stratified into three subgroups depending on the degree of left ventricular systolic dysfunction, as assessed during their hospitalization for MI. Subsequently, the 30-day, 12-month, and 36-month outcomes in the diabetic study subgroups were compared with those in the corresponding non- -diabetic subgroups. This analysis encompassed a nationwide cohort of 58 123 patients. Twelve- and 36-months mortality was greater in diabetic patients than in non-diabetic patients. The highest 36-months mortality (46.64%) was in the group of patients with DM and reduced ejection fraction (EF) <40%. Multivariate analysis showed diabetes and low EF to be independent risk factors for 36-month mortality, increasing the risk of death by 35% for diabetes and by 30% for each 5-percentage point EF decrease. Higher mortality was observed in older patients, smokers, and patients with ischemic heart disease before the index hospitalization. Both diabetes and reduced EF proved to be independent risk factors for increased mortality over a long-term follow-up after MI.

The evolving characteristics and outcomes of acute myocardial infarction in Hong Kong, 1999–2018

Abstract Background The burden of myocardial infarction (MI) with its assorted comorbid complications is increasing parallel to rising life expectancy. Careful characterisation of patient characteristics and identification of short- and long-term complications is critical to their management. Nonetheless, data on the evolving profiles of patient features and outcomes, particularly in an Asian population, remain sparse. Purpose We aim to describe the evolving characteristics and outcomes of MI patients in Hong Kong in the past 2 decades. Methods From a well-validated territory-wide database in Hong Kong, we included patients with incident acute MI from 1999/01/01 to 2018/12/31. The primary outcome was 30-day all-cause death, while secondary outcomes include haemorrhagic stroke, and pneumonia, at both 30 days and 5 years. Temporal trends in baseline characteristics were evaluated using Poisson regression, while trends in outcomes were evaluated using Cox proportional hazard model, adjusted with demographics, comorbidities, and baseline medications. Results A total of 130,218 patients (age 73.6±13.9 years, 40.0% female) were included. Over time, while there was no change in the proportion of females (P=0.196), the increase in mean age (APC 0.23% [0.21 to 0.24], P&amp;lt;0.001) was concordant with the increase in mean CCI (APC 5.1%, [4.8 to 5.3], P&amp;lt;0.001), with more patients suffering from baseline comorbidities (Figure 1; range of APC 1.7% to 4.3%; all P&amp;lt;0.001). The proportion of ST elevation increased significantly (APC 2.5% [2.4 to 2.5], P&amp;lt;0.001). The adjusted all-cause 30-day mortality rate decreased increased significantly (APC 0.3% [0.1 to 0.5], P=0.005). The increasing trend was significant in older patients (≥70 years), non-ST elevation, and female, while there was a decreasing trend mortality rate in ST elevation and young patients; no significant trend was observed in male. Strikingly, there is an alarming increase in the rate of haemorrhagic stroke (APC 3.4% [2.3 to 4.4], P&amp;lt;0.001) and pneumonia (APC 1.5% [1.3 to 1.7], P&amp;lt;0.001) at 30 days (Figure 2). Although the rate of 5-year all-cause death declined slightly (APC −0.8% [−0.9 to −0.6], P&amp;lt;0.001), there were increasing rates of haemorrhagic stroke (APC 1.0% [0.3 to 1.7], P=0.004) and pneumonia (APC 3.8% [3.6 to 4.1], P&amp;lt;0.001). Patients who were older, had ST elevation, and more comorbid were more likely to develop pneumonia. Conclusions Patients with MI have evolved to be older and more comorbid. Alarmingly, despite reduction in long-term all-cause death over time, the reduction was small; risk of death in short-term significantly increased and patients suffer from more complications including haemorrhagic stroke and pneumonia. These results highlight the emergence of extra-cardiac outcomes that drive poor prognosis and accentuate the need to develop tailored strategies to tackle these potentially lethal complications. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): The Shenzhen Key Medical Discipline; The Sanming Project of HKU-SZH Cardiology

IN-HOSPITAL BLOOD PRESSURE VARIABILITY AS A PREDICTOR OF LONG-TERM CARDIOVASCULAR MORTALITY IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION: ONE-YEAR FOLLOW-UP STUDY

Abstract Objective: The impact of blood pressure variability (BPV) on cardiovascular morbidity and mortality has been examined through the prism of heart failure and hypertension, but not in the setting of myocardial infarction (MI). The aim of this study is to determine the association between in-hospital short-term BPV and long-term cardiovascular outcomes in MI patients. Design and method: A total population of 260 patients (82.2% male; mean age: 63.8 years;71.3% hypertensives, 48.1% STEMI)underwent 24-hambulatory BP measurement during hospitalization for MI. At one year a follow-up was scheduled in order to assesscardiovascular mortality. The parameters of BPV analyzed were: a) 24-h standard deviation (SD), b) the coefficient of variation (CV) and c) the average real variability (ARV) of systolic and diastolic BP. Results: Cardiovascular death was independently predicted by SD SBP (HR = 2.406; 95% CI: 0.865–3.947; P = 0.002)and CV SBP (HR = 3.093; 95% CI: 1.833–4.354; P &lt; 0.001) in the entire population and separately in STEMI group[(HR = 5.485; 95% CI: 2.958–8.012; P &lt; 0.001) and (HR = 5.521; 95% CI: 3.230–7.813; P &lt; 0.001) respectively]but not in the NSTEMI one. ARV failed to predict mortality in either group or the entire population. Multivariate regression models were conducted for both SD SBP and CV SBP in the STEMI group,in which, both remained potent predictors of cardiovascular mortality independently ofgender, age, hypertension, DM, smoking, low density lipoprotein (LDL-C) andGFR[(HR = 6.131; 95% CI: 3.716–8.546; P &lt; 0.001) and (HR = 5.870; 95% CI:3.609–8.131; P &lt; 0.001) respectively]. Conclusions: In the setting of MI, in-hospital BPV was associated with cardiovascular mortality during the one-year follow-up. These findingscould suggest a clinical need for further individualization of BP regulation in the integrative ACS management.

Association between smoking status and outcomes in myocardial infarction patients undergoing percutaneous coronary intervention

Smoking is one of the leading risk factors for cardiovascular diseases, including ischemic heart disease and hypertension. However, in acute myocardial infarction (AMI) patients, smoking has been associated with better clinical outcomes, a phenomenon termed the “smoker’s paradox.” Given the known detrimental effects of smoking on the cardiovascular system, it has been proposed that the beneficial effect of smoking on outcomes is due to age differences between smokers and non-smokers and is therefore a smoker’s pseudoparadox. The aim of this study was to evaluate the association between smoking status and clinical outcomes in ST-segment elevation (STEMI) and non-STEMI (NSTEMI) patients treated by percutaneous coronary intervention (PCI), using a national multi-ethnic Asian registry. In unadjusted analyses, current smokers had better clinical outcomes following STEMI and NSTEMI. However, after adjusting for age, the protective effect of smoking was lost, confirming a smoker’s pseudoparadox. Interestingly, although current smokers had increased risk for recurrent MI within 1 year after PCI in both STEMI and NSTEMI patients, there was no increase in mortality. In summary, we confirm the existence of a smoker’s pseudoparadox in a multi-ethnic Asian cohort of STEMI and NSTEMI patients and report increased risk of recurrent MI, but not mortality, in smokers.

Angiographic predictors of outcome in myocardial infarction patients presenting with cardiogenic shock: a CULPRIT-SHOCK angiographic substudy.

The aim of this study was to determine the prognostic impact of pre- and post-PCI TIMI flow grade and TIMI myocardial perfusion grade (TMPG) in a well-defined group of patients with cardiogenic shock due to acute myocardial infarction. Patients with infarct-related cardiogenic shock randomised into the CULPRIT-SHOCK trial were included in the angiographic predictor analysis whenever their TIMI flow grade or TMPG was available in the core lab database (96.9% of cases). A multivariable logistic regression analysis, adjusted on non-angiographic covariates, was performed to investigate whether TIMI flow grade or TMPG was independently associated with all-cause mortality or renal replacement therapy up to one year. Pre-PCI TIMI flow grade and TMPG did not impact on mortality. When analysed in separate multivariable models, post-PCI TIMI 3 flow and TMPG grade 3 were both significantly associated with reduced risk of 30-day mortality: aOR 0.61 (95% CI: 0.38-0.97, p=0.037) and 0.46 (95% CI: 0.29-0.72, p<0.001), respectively. When considered in the same multivariable model, only TMPG was significantly associated with 30-day mortality (aOR 0.38 [0.20-0.71], p=0.002), the 30-day composite of all-cause mortality and renal replacement therapy (aOR 0.34 [0.18-0.66], p=0.001) and mortality at one-year follow-up (aOR 0.46 [0.24-0.88], p=0.02). Post-PCI TIMI flow grade and TMPG are associated with mortality after PCI. TMPG is a better discriminator, supporting microcirculation rather than epicardial reperfusion for prognosis estimation.

Comparison of Outcomes with or without Beta-Blocker Therapy After Acute Myocardial Infarction in Patients Without Heart Failure or Left Ventricular Systolic Dysfunction (from the Acute Coronary Syndromes Israeli Survey [ACSIS

The contemporary benefit of routine beta-blocker therapy following myocardial infraction in the absence of heart failure or left ventricular systolic dysfunction is unclear. We investigated the impact of beta-blockers on post myocardial infarction outcome in patients without heart failure or left ventricular systolic dysfunction among patients enrolled in the biennial Acute Coronary Syndrome Israeli Surveys. MACE rates at 30 days and overall mortality at one year were compared among patients discharged on beta-blockers versus not, after multivariate analysis to adjust for baseline differences. Between the years 2000 to 2016, data from 15.211consecutive ACS patients were collected. Of 7,392 patients who met the inclusion criteria, 6007 (79.9%) were discharged on beta-blocker therapy. Prescription of beta-blockers at discharge increased modestly from 32% to 38% over the 16-year period. The 30-day MACE rates were similar in patients on vs. not on beta-blockers at discharge (9.0% and 9.5%, respectively). One year survival did not differ significantly between those on vs. not on beta-blockers (HR 0.8, 95% CI 0.58 to 1.11, p = 0.18).In conclusion, beta-blocker therapy did not affect 30 days MACE or 1-year survival after myocardial infarction in patients without heart failure or reduced ejection fraction.

Inhibition of the long non-coding RNA NEAT1 protects cardiomyocytes from hypoxia in vitro via decreased pri-miRNA processing

While restoration of coronary blood flow to the ischemic heart is the most effective strategy for reducing infarct size, reperfusion injury represents a significant limiting factor on clinical outcomes in myocardial infarction patients. Ischemic preconditioning (IPC) has been shown to inhibit reperfusion injury and represents an attractive model for studying cardioprotective signal transduction pathways. Long non-coding RNAs (lncRNAs) are a structurally and functionally heterogenous class of RNA transcripts with unknown roles in IPC-induced cardioprotection. Through microarray-based expression profiling of 31,423 lncRNAs in cardiac tissue from IPC mice, we identified the nuclear transcript Neat1 to be rapidly and robustly decreased in response to IPC. siRNA-mediated knock down of Neat1 reduced apoptosis and necrosis in murine cardiomyocytes (CM) and human iPS-derived CMs in response to prolonged hypoxia and hypoxia-reoxygenation, assessed with Annexin V/propidium iodide-staining, a Caspase 3/7 activity assay, LDH release, and western blot for cleaved Caspase 3. Mechanistically, Neat1 was shown to regulate processing of pro-apoptotic microRNA-22 (miR-22) in murine and human CM nuclei using a luciferase reporter assay. Hypoxia-induced downregulation of Neat1 was shown to result in accumulation of unprocessed pri-miRNA and decreased availability of biologically active miRNA, including miR-22. Addition of exogenous synthetic miR-22 reversed the protective effect of Neat1 knock down in human iPS-CM. In conclusion, we have identified the nuclear lncRNA Neat1 as part of a conserved oxygen-sensitive feedback mechanism by regulation of miRNA processing and a potential target in cardioprotection.

Correlation between Galectin-3 and Adverse Outcomes in Myocardial Infarction Patients: A Meta-Analysis.

Background Acute myocardial infarction (AMI) is a disease with high morbidity and mortality. Some new biomarkers can help us to improve the life quality and prognosis of AMI patients. Objective We therefore performed a systematic review and meta-analysis on the use of galectin-3 (gal3) for assessing prognosis of AMI patients. Methods We searched Medline, Embase, Web of Science, Cochrane Library, SinoMed, China National Knowledge Infrastructure (CNKI), and Wanfang database up to June 2019. Trials included using galectin-3 to estimate prognosis in myocardial infarction (MI) patients. Results We identified 10 trails with a total of 2809 participants. The negative correlation between galectin-3 and left ventricular ejection fraction (LVEF) was significant in 505 AMI patients (Fisher's Z −0.22, 95% CI: −0.34, −0.09). The correlation between galectin-3 and infarct size was not significant in 119 patients (Fisher's Z 0.12, 95% CI: −0.36, 0.60). Higher galectin-3 was associated with increased all-cause mortality in 2343 AMI patients (Fisher's Z 1.58, 95% CI: 1.23, 2.03). Conclusion The limited evidence suggests that galectin-3 is likely to predict the adverse outcomes in MI patients, but it is not significantly correlated with infarct size after MI. More high-quality trials with longer-term follow-up are still needed to confirm this finding.

The association between anxiety disorders and in-hospital outcomes in patients with myocardial infarction.

BackgroundAnxiety disorders are prevalent in patients with myocardial infarction (MI), but the effects of anxiety disorders on in‐hospital outcomes within MI patients have not been well studied.HypothesisTo examine the effects of concurrent anxiety disorders on in‐hospital outcomes in MI patients.MethodsWe conducted a retrospective cohort study in patients with a principal diagnosis of MI with and without anxiety disorders in the National Inpatient Sample 2016. A total of 129 305 primary hospitalizations for acute MI, 35 237 with ST‐segment elevation myocardial infarction (STEMI), and 94 068 with non‐ST elevation myocardial infarction (NSTEMI) were identified. Of these, 13 112 (10.1%) had anxiety (7.9% in STEMI and 11.0% in NSTEMI). We compared outcomes of anxiety and nonanxiety groups after propensity score matching for the patient and hospital demographics and relevant comorbidities.ResultsAfter propensity score matching, the anxiety group had a lower incidence of in‐hospital mortality (3.0% vs 4.4%, P < .001), cardiac arrest (2.1% vs 2.8%, P < .001), cardiogenic shock (4.9% vs 5.6%, P = .007), and ventricular arrhythmia (6.7% vs 7.9%, P < .001) than the nonanxiety group. In the NSTEMI subgroup, the anxiety group had significantly lower rates of in‐hospital mortality (2.3% vs 3.5%, P < .001), cardiac arrest (1.1% vs 1.5%, P = .008), and cardiogenic shock (2.8% vs 3.5%, P = .008). In the STEMI subgroup, we found no differences in in‐hospital outcomes (all P > .05) between the matched groups.ConclusionAlthough we found that anxiety was associated with better in‐hospital outcomes, subgroup analysis revealed that this only applied to patients admitted for NSTEMI instead of STEMI.

Abstract 491: Small Gtpase Rhoe Regulates Inflammatory Response in Myocardial Infarction

Background: Myocardial infarction (MI) is a severe clinical condition caused by coronary artery thrombotic occlusion. An acute inflammatory response to MI is essential for cardiac healing, while excessive and prolonged inflammation causes cytotoxic damages and provokes adverse cardiac remodeling. In the present study, we demonstrate a novel inflammatory mediator, RhoE, and its cardioprotective role in MI. Methods: We use three genetic mouse lines in this study: global RhoE knockout, cardiac-specific RhoE haploinsufficient, and cardiac-specific RhoE overexpression mice. Cardiac function and inflammation in the first week post MI are assessed in mice receiving left anterior descending artery (LAD) ligation. Mechanistic study is conducted through a set of molecular signaling experiments including bimolecular fluorescence complementation (BiFC), immunoprecipitation, electrophoretic mobility shift assay and mRNA microarray analysis. Finally, we investigate the expression and clinical significance of RhoE in MI patients. Results: RhoE is upregulated in mouse post MI. RhoE deletion leads to upregulation of pro-inflammatory genes in mouse embryo heart. RhoE haploinsufficiency causes excessive inflammatory response with deleterious cardiac function post MI, while RhoE overexpression restrains post-MI inflammation and preserves cardiac function and survival. Mechanistically, RhoE specifically inhibits NF- κB activation in vivo and in vitro. RhoE binds to p65 and p50 individually in cytosol, blocking their dimerization and nuclear translocation. Consistent with findings in the mouse MI model, MI patients with higher RhoE expression show diminished cardiac inflammation and consequently a better prognosis. Conclusions: This study identified RhoE as a fine-tuning factor modulating post-MI inflammation. RhoE expression level in heart positively correlates with the outcomes of MI patients. Impact: The discovery of RhoE provides a potential therapeutic target for MI. RhoE abundance in the heart post-MI might be used for prognosis assessment.

Relationship of obesity to adverse events in myocardial infarction patients without primary percutaneous coronary intervention: results from the Occluded Artery Trial (OAT)

Objective: Our goal was to investigate the “obesity paradox” in myocardial infarction populations without primary percutaneous coronary intervention (PPCI).Methods: The Occluded Artery Trial (OAT, Clinicaltrials.gov: NCT00004562) is a randomized, multicenter study to investigate the influence of routine percutaneous coronary intervention (PCI) on the clinical outcomes of myocardial infarction patients without PPCI. We stratified these patients into three groups according to body mass index (BMI): normal, 18.5 kg/m2 ≤ BMI < 25 kg/m2; overweight, 25 kg/m2 ≤ BMI < 30 kg/m2; obese, BMI ≥ 30 kg/m2. The purpose of our study was to investigate the effects of BMI on the primary endpoint (all-cause mortality) and the secondary endpoint (cardiac death, non-cardiac death or New York Heart Association [NYHA] class IV heart failure) in the population enrolled in the OAT.Results: A total of 2153 patients (99.4%) constituted the final study population. We found that obese patients were younger and were more likely to have cardiovascular risk factors compared with other BMI groups. A U-shaped relationship was observed between BMI and all-cause mortality. The adjusted hazard ratios (HRs) were 0.892 (95% CI: 0.658–1.210, p = .460) for normal weight patients and 0.671 (95% CI: 0.508–0.888, p = .013) for overweight patients compared with obese patients. The same pattern was also observed for non-cardiac death. The adjusted HRs were 0.919 (95% CI: 0.601–1.40, p = .663) for normal weight patients and 0.524 (95% CI: 0.346–0.792, p = .004) for overweight patients compared with obese patients. We did not find any statistical differences among BMI categories in terms of cardiac death or NYHA class IV heart failure.Conclusions: A U-shaped relationship was observed between BMI and all-cause mortality or non-cardiac death. Overweight patients have the lowest risk of all-cause mortality, which may be attributed to their having the lowest risk of non-cardiac death of the groups studied.