Onset Of Myocardial Infarction Research Articles

Abstract 4137359: Electrocardiographic ST–T area assessed by a computerized quantitative method were associated with increased risk of cardiovascular disease, especially ischemic stroke, in patients with cardiovascular risk factor

Background: ST changes in the lateral leads, which reflect ischemic changes, are associated with cardiovascular events. However, quantitative assessment of the ST–T area and its association with cardiovascular events remains unclear. Hypothesis: Electrocardiographic ST–T areas in lateral leads (V5 and V6) quantitatively assessed by machine analysis were associated with cardiovascular events. Methods: We enrolled 4,654 subjects from the Cardiovascular Prognostic Coupling Study in Japan (Coupling Registry), who had one or more cardiovascular risk factors. The primary endpoint was composite (cardiovascular death, myocardial infarction, stroke), and the secondary endpoints were myocardial infarction and stroke. ST–T area was assessed as the area enclosed by the baseline from the end of the QRS complex to the end of the ST–T segment using a computerized quantitative method. We used the lower magnitude of ST–T area in the V5 or V6 lead for the analysis. The endpoints were compared between the lowest quartile of ST–T area (Q4) and the others (Q1–3). Results: The mean follow-up period was 53 ± 17 months. The composite endpoint was 159 cases, myocardial infarction in 27 cases and cerebral infarction in 72 cases. The lowest quartile of ST–T area (N= 1,162) had significantly more cardiovascular events than the other Q1–3 groups (N= 3,492, hazard ratio [HR] 2.25, 95% confidence interval [CI] 1.64–3.10) after adjusting for age, gender, and other covariates. The onset of myocardial infarction did not reach statistical difference (HR 2.05, 95% CI 0.94–4.46, p=0.072), but the lowest quartile of ST–T area significantly more ischemic stroke than the other Q1–3 groups (HR 2.37, 95% CI 1.48–3.75 p<0.001) Conclusions: The lower summations of ST–T area assessed by a computerized quantitative method were associated with increased risk of cardiovascular disease, especially ischemic stroke, in patients with one or more cardiovascular risk factors.

Abstract 4119327: Tyrosine Kinase Inhibitor and Their Cardiotoxic Profile in the African American Population at a Community Safety Net Hospital

Intro: Tyrosine Kinase inhibitors (TKI) have been an effective treatment option for multiple cancer types. Unfortunately, TKIs have shown to have off-target Kinase binding to cardiac tissue. The examination of these cardiotoxic side effects have not been sufficiently explored in minority populations and studies such as DASISION and ENESTnd with high NAA homogeneous demographics reflect this issue. AA tend to have higher rates of HTN and HF at baseline, so further evaluation of TKI cardiotoxicity in this population is warranted. Methods: A total of 181 patients (pts) charts were reviewed in this study, who were exposed to either Ibrutinib, Imatinib and Sorafenib. First, Patients’ demographic data, such as age, gender, race, malignancy type were obtained along with their corresponding exposure to TKIs discussed above. Next, each patient (pt) chart was examined for any cardiotoxic etiologies after starting a TKI, such as arrhythmias, new- onset heart failure (nOHF) , cardiac arrest (CA), and Myocardial infarction (MI). Echocardiography reports were examined for Ejection fraction ( EF). In summary, this is an observational study looking at Cardiotoxicity secondary to TKI use in the AA population. Results: This study's demographics consisted of 149 AA and 32 NAA (non- african american), with the average age of 64.2, and had 128 males and 53 females. A total of 89 pts were on imatinib, 57 on Ibrutinib, 35 on sorafenib. In our population, 64 pts received cardiac echography while on TKIs, with 9 of them demonstrating nOHF. In terms of cardiac arrhythmias, a total of 67 pts experienced this while on TKI, with about 34% (51/149) of AA compared to 50% (16/32) of NAA. A total of 18 pts in the study required hospital management as a sequelae of their cardiotoxicity. Conclusion: There were a few trends that diverged from most studies regarding cardiotoxicity associated with TKIs in our study. When looking at individual items, such as rate of Atrial Fibrillation (AF), seen commonly in patients on Ibrutinib, our rate seen is 4.6% which is lower compared to earlier pooled homogenous population studies (6-7%). Earlier clinical trials of Sorafenib had a 2 % rate of HF in mostly homogenous NAA populations, and our study had 0% rate in total. Overall, several cardiotoxicity trends seen with the TKIs in this observational study warrant need for future studies to enable improved cardiac surveillance strategies post treatment in heterogeneous populations.

Abstract 4138407: Exome-wide association study of over a million individuals identified effector genes and variants for blood lipids

Background: Inherited hypercholesterolemia is an important Mendelian condition associated with early onset myocardial infarction. However, current genetic diagnostic criteria only partially explain severe clinical hypercholesterolemia. Furthermore, current pathogenicity categorizations do not consistently inform prognosis, but quantification is limited by scarcity of such rare variants. Aim: Exploiting populations scale genotype/phenotype data, to determine the architecture of the genetic variants associating with blood lipid levels with quantitative assessments. Methods: Here, we discovered and characterized rare coding alleles contributing to genetic dyslipidemia, a principal risk for coronary artery disease, among over a million individuals combining two large contemporary genetic datasets (Million Veteran Program N = 626,554 and UK Biobank, N = 431,026). Results: Testing 2,869,269 rare (minor allele frequency < 1%), coding variants, we identified 793 exome-wide significant associations ( P < 4.4 × 10 -11 ), including 8 previously undiscovered loci. Associated alleles are highly enriched in functional variant classes; high confidence predicted loss of function, deleterious missense, and cryptic splicing, showed significant and recessive associations, had similar effects across populations. Overall, rare variants contributed to additional > 16% of genetic trait variances on top of common genetic variants. The effect estimates of associated signals confirmed and refined curated pathogenic database, highlighted by the identification of African or South Asian specific pathogenic alleles previously controversial in its pathogenicity. Conclusion: This study provides resources and insights for understanding causal mechanisms and quantifying the expressivity of rare coding alleles for blood lipids by large scale sequencing study. Furthermore, identifying and characterizing population enriched variants, our study underscored the importance of multi-population rare variant study.

Le coroscanner peut-il être réalisé en dépistage à grande échelle en prévention des syndromes coronaires aigus et de l'insuffisance cardiaque ischémique ?

Coronary CT-Scan permits non-invasive visualization of all stages of coronary artery atherosclerosis allowing early therapeutic interventions, lifestyle changes and accurate follow-up all of which result in an improved prognosis. We discuss the possibility of a systematic coronary CT-scan in the global population at certain ages such as fifty or sixty years-old (or both). May this strategy decrease the onset of myocardial infarction or ischemic chronic heart failure thus improving quality (and quantity) of life? May it also reduce the medical costs for the individual and the society? Is it technically possible to deploy such a strategy? What would be the obstacles for its set up and what solutions might be proposed?

Deficiency of transcription factor E4BP4 suppresses neointimal formation after vascular injury

Abstract Aim In addition to traditional risk factors such as hypertension, diabetes, and dyslipidemia, chronic inflammation is deeply involved in the onset and pathogenesis of atherosclerotic diseases. Furthermore, diurnal fluctuations are observed in the rupture of atherosclerotic plaques and the onset of myocardial infarction. There are still many patients for whom medical treatments such as statins and antihypertensive drugs do not respond adequately, and new treatment methods are expected. E4BP4 (also known as NFIL3) is a basic leucine zipper (bZIP)-type transcription factor associated with circadian rhythms and cell viability, and it has been reported that E4BP4 regulates inflammation. Therefore, to investigate how the circadian transcription factor E4BP4 which is involved in inflammation, we decided to examine the role of E4BP4 in neointimal formation after vascular injury. Methods and Results Using E4BP4-deficient (E4BP4−/−) and wild-type (WT) mice, we investigated neointimal formation 2 weeks after femoral artery injury induced by an external vascular cuff model. Intimal and medial area were measured, and the intima/media ratio was calculated. Systolic blood pressure was similar between groups (WT mice: 92 ± 5 mmHg [n = 5] vs. E4BP4−/− mice: 90 ± 4 mmHg [n = 5]). And there was no significant difference in baseline body weight between groups (WT mice: 22.4 ± 0.8 g [n = 5] vs. E4BP4−/− mice: 22.0 ± 1.1 g [n = 5]). The mean intimal area and the intima/media ratio of E4BP4−/− mice decreased by 86 % (WT mice: 3,683 ± 512 μm2 [n = 10] vs. E4BP4−/− mice: 521 ± 363 μm2 [n = 10]; P < 0.0001) and 97% (WT mice: 0.33 ± 0.05 vs. E4BP4−/− mice: 0.01 ± 0.03; P < 0.0001), compared with WT mice. However, we observed no significant difference in the medial area (WT mice: 11,019 ± 358 μm2 vs. E4BP4−/− mice: 11,281 ± 401 μm2; P = NS) between groups (Figure). Immunohistochemistry for NK cell (NKp46) revealed the percentage of NKp46 positive area in the adventitia of E4BP4−/− mice was significantly lower compared with WT mice at 14 days post-injury (P <0.05). Furthermore, the positive area of IL-6 (P<0.05), TNF-α (P<0.05) and IFN-γ (P<0.05) in the intima of E4BP4−/− mice tended to be much smaller than those of WT mice. Our findings indicate that E4BP4 might induce vascular inflammation following vascular injury. Conclusions Deficiency of E4BP4 reduced the inflammatory cytokines and suppressed neointimal formation after injury. We also observed a decrease in NKp46, suggesting that NK cell development is impaired by E4BP4 deficiency. The present study is the first to demonstrate that E4BP4 plays an important role in the increase of neointimal formation after injury in vivo, thus suggesting that E4BP4 inhibition may represent a useful strategy to inhibit vascular inflammation.Neointimal formation after cuff injury

Low ambient temperature and incident myocardial infarction with or without obstructive coronary arteries: a Chinese nationwide study.

Although non-optimum ambient temperature is a major non-traditional risk factor for acute myocardial infarction, there is no prior knowledge on whether non-optimum ambient temperature could differentially affect myocardial infarction with obstructive coronary artery disease (MI-CAD) and myocardial infarction with non-obstructive coronary arteries (MINOCA). Using the Chinese Cardiovascular Association database-Chest Pain Center Registry, a nationwide, time-stratified, case-crossover investigation was conducted from 2015 to 2021. Meteorological data were obtained from an established satellite-based model, and daily exposures were assigned according to the onset of myocardial infarction in each patient. A conditional logistic regression model combined with distributed lag non-linear models (10 days) was used to estimate the exposure-response relationships. A total of 83 784 MINOCA patients and 918 730 MI-CAD patients were included. The risk of MINOCA and MI-CAD associated with low temperature occurred at lag 2 day and lasted to 1 week. Extremely low temperature was associated with a substantially greater odds ratio (OR) of MINOCA [OR 1.58, 95% confidence interval (CI) 1.31-1.90] than MI-CAD (unmatched: OR 1.32, 95% CI 1.23-1.43; equally matched by age and sex: OR 1.25, 95% CI 1.04-1.50), compared with the corresponding reference temperatures (30°C, 35°C, and 30°C). Stronger associations were observed for patients who were aged ≥65 years, female, or resided in the south. There was no significant difference for the impacts of high temperature on MINOCA and MI-CAD. This nationwide study highlights the particular susceptibility of MINOCA patients to ambient low temperature compared with that of MI-CAD patients.

Exposure to Air Pollutants and Myocardial Infarction Incidence: A UK Biobank Study Exploring Gene-Environment Interaction.

Unraveling gene-environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population. We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence. This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution (, , , and ) from the UK Department for Environment, Food and Rural Affairs (2006-2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales. Among 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for , 1.20 (95% CI: 1.19, 1.22) for , 1.13 (95% CI: 1.12, 1.15) for , and 1.12 (95% CI: 1.11, 1.13) for . In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants ( to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI. There were interactions between exposure to ambient air pollutants and genetic susceptibility on the risk of MI onset. Moreover, the joint effects of these two exposures were greater than the effect of each factor alone. https://doi.org/10.1289/EHP14291.

The Role of Inflammation in the Pathogenesis of Cardiogenic Shock Secondary to Acute Myocardial Infarction: A Narrative Review.

Cardiogenic shock (CS) is one of the most serious complications of myocardial infarction (MI) with a high mortality rate. The timely and effective prevention and early suppression of this adverse event may influence the prognosis and outcome in patients with MI complicated by CS (MI CS). Despite the use of existing pharmaco-invasive options for maintaining an optimal pumping function of the heart in patients with MI CS, its mortality remains high, prompting the search for new approaches to pathogenetic therapy. This review considers the role of the systemic inflammatory response in the pathogenesis of MI CS. The primary processes involved in its initiation are described, including the progression from the onset of MI to the generalization of the inflammatory response and the development of multiple organ dysfunction. The approaches to anti-inflammatory therapy in patients with CS are discussed, and further promising research directions are outlined. In this review, we updated and summarized information on the inflammatory component of MI CS pathogenesis with a particular focus on its foundational aspects. This will facilitate the identification of specific inflammatory phenotypes and endotypes in MI CS and the development of targeted therapeutic strategies for this MI complication.

A systematic review and meta-analysis of differences between men and women in short-term outcomes following coronary artery bypass graft surgery

We provide an update regarding the differences between men and women in short-term postoperative mortality after coronary artery bypass grafting (CABG) and highlight the differences in postoperative risk of stroke, myocardial infarction, and new onset atrial fibrillation. We included 23 studies, with a total of 3,971,267 patients (70.7% men, 29.3% women), and provided results for groups of unbalanced studies and propensity matched studies. For short-term mortality, the pooled odds ratio (OR) from unbalanced studies was 1.71 (with 95% CI 1.69–1.74, I2 = 0%, p = 0.7), and from propensity matched studies was 1.32 (95% CI 1.14–1.52, I2 = 76%, p < 0.01). For postoperative stroke, the pooled effects were OR = 1.50 (95% CI 1.35–1.66, I2 = 83%, p < 0.01) and OR = 1.31 (95% CI 1.02–1.67, I2 = 81%, p < 0.01). For myocardial infarction, the pooled effects were OR = 1.09 (95% CI = 0.78–1.53, I2 = 70%, p < 0.01) and OR = 1.03 (95% CI = 0.86–1.24, I2 = 43%, p = 0.18). For postoperative atrial fibrillation, the pooled effect from unbalanced studies was OR = 0.89 (95% CI = 0.82–0.96, I2 = 34%, p = 0.18). The short-term mortality risk after CABG is higher in women, compared to men. Women are at higher risk of postoperative stroke. There is no significant difference in the likelihood of postoperative myocardial infarction in women compared to men. Men are at higher risk of postoperative atrial fibrillation after CABG.

Significance of Nitric Oxide Derived from the Nitric Oxide Synthases System in Cardiovascular Inter-Organ Cross-Talk.

Inter-organ cross-talk contributes to the pathogenesis of various disorders, and drug development based on inter-organ cross-talk is attracting attention. The roles of nitric oxide (NO) derived from the NO synthases system (NOSs) in inter-organ cross-talk remain unclear. We have investigated this issue by using our mice deficient in all three NOSs (triple n/i/eNOSs-/- mice). We reported that 2/3 nephrectomized triple n/i/eNOSs-/- mice die suddenly because of early onset of myocardial infarction, suggesting the protective role of NO derived from NOSs in the cross-talk between the kidney and the heart. We studied the role of NO derived from NOSs expressed in the bone marrow in vascular lesion formation. Constrictive arterial remodeling and neointimal formation following unilateral carotid artery ligation were prominently aggravated in wild-type mice transplanted with triple n/i/eNOSs-/- bone marrow cells as compared with those with wild-type bone marrow cells, suggesting the protective role of NO derived from NOSs in the cross-talk between the bone marrow and the blood vessel. We further investigated the role of NO derived from NOSs expressed in the bone marrow in pulmonary hypertension. The extent of pulmonary hypertension after chronic hypoxic exposure was markedly exacerbated in wild-type mice underwent triple n/i/eNOSs-/- bone marrow transplantation as compared with those underwent wild-type bone marrow transplantation, suggesting the protective role of NO derived from NOSs in the cross-talk between the bone marrow and the lung. These lines of evidence demonstrate that systemic and myelocytic NOSs could be novel therapeutic targets for myocardial infarction, vascular disease, and pulmonary hypertension. Significance Statement We demonstrated in studies with triple n/i/eNOSs-/- mice that partial nephrectomy accelerates the occurrence of myocardial infarction induced by systemic NOSs deficiency, that myelocytic NOSs deficiency aggravates vascular lesion formation after unilateral carotid artery ligation, and that myelocytic NOSs deficiency exacerbates chronic hypoxia-induced pulmonary hypertension. These results suggest that NO derived from NOSs plays a protective role in cardiovascular inter-organ cross-talk, indicating that systemic and myelocytic NOSs could be important therapeutic targets for myocardial infarction, vascular disease, and pulmonary hypertension.

The role of antiphospholipid antibodies in the onset of myocardial infarction

The role of antiphospholipid antibodies in the onset of myocardial infarction

Short-term association between ambient ozone and onset of acute myocardial infarction of young patients: Results from the VIRGO study

Short-term association between ambient ozone and onset of acute myocardial infarction of young patients: Results from the VIRGO study

A Comparison of Interpretable Machine Learning Approaches to Identify Outpatient Clinical Phenotypes Predictive of First Acute Myocardial Infarction.

Acute myocardial infarctions are deadly to patients and burdensome to healthcare systems. Most recorded infarctions are patients' first, occur out of the hospital, and often are not accompanied by cardiac comorbidities. The clinical manifestations of the underlying pathophysiology leading to an infarction are not fully understood and little effort exists to use explainable machine learning to learn predictive clinical phenotypes before hospitalization is needed. We extracted outpatient electronic health record data for 2641 case and 5287 matched-control patients, all without pre-existing cardiac diagnoses, from the Michigan Medicine Health System. We compare six different interpretable, feature extraction approaches, including temporal computational phenotyping, and train seven interpretable machine learning models to predict the onset of first acute myocardial infarction within six months. Using temporal computational phenotypes significantly improved the model performance compared to alternative approaches. The mean cross-validation test set performance exhibited area under the receiver operating characteristic curve values as high as 0.674. The most consistently predictive phenotypes of a future infarction include back pain, cardiometabolic syndrome, family history of cardiovascular diseases, and high blood pressure. Computational phenotyping of longitudinal health records can improve classifier performance and identify predictive clinical concepts. State-of-the-art interpretable machine learning approaches can augment acute myocardial infarction risk assessment and prioritize potential risk factors for further investigation and validation.

Genetics of Cardiac Aging Implicate Organ-Specific Variation.

Heart structure and function change with age, and the notion that the heart may age faster for some individuals than for others has driven interest in estimating cardiac age acceleration. However, current approaches have limited feature richness (heart measurements; radiomics) or capture extraneous data and therefore lack cardiac specificity (deep learning [DL] on unmasked chest MRI). These technical limitations have been a barrier to efforts to understand genetic contributions to age acceleration. We hypothesized that a video-based DL model provided with heart-masked MRI data would capture a rich yet cardiac-specific representation of cardiac aging. In 61,691 UK Biobank participants, we excluded noncardiac pixels from cardiac MRI and trained a video-based DL model to predict age from one cardiac cycle in the 4-chamber view. We then computed cardiac age acceleration as the bias-corrected prediction of heart age minus the calendar age. Predicted heart age explained 71.1% of variance in calendar age, with a mean absolute error of 3.3 years. Cardiac age acceleration was linked to unfavorable cardiac geometry and systolic and diastolic dysfunction. We also observed links between cardiac age acceleration and diet, decreased physical activity, increased alcohol and tobacco use, and altered levels of 239 serum proteins, as well as adverse brain MRI characteristics. We found cardiac age acceleration to be heritable (h2g 26.6%); a genome-wide association study identified 8 loci related to linked to cardiomyopathy (near TTN, TNS1, LSM3, PALLD, DSP, PLEC, ANKRD1 and MYO18B) and an additional 16 loci (near MECOM, NPR3, KLHL3, HDGFL1, CDKN1A, ELN, SLC25A37, PI15, AP3M1, HMGA2, ADPRHL1, PGAP3, WNT9B, UHRF1 and DOK5). Of the discovered loci, 21 were not previously associated with cardiac age acceleration. Mendelian randomization revealed that lower genetically mediated levels of 6 circulating proteins (MSRA most strongly), as well as greater levels of 5 proteins (LXN most strongly) were associated with cardiac age acceleration, as were greater blood pressure and Lp(a). A polygenic score for cardiac age acceleration predicted earlier onset of arrhythmia, heart failure, myocardial infarction, and mortality. These findings provide a thematic understanding of cardiac age acceleration and suggest that heart- and vascular-specific factors are key to cardiac age acceleration, predominating over a more global aging program.

Managing the Intricacies of Coronary Revascularization: A Close Look at the Complete Versus Culprit-Only Approach and its Implications in Elderly Patients.

Coronary heart disease is the leading cause of mortality in the United States, and data indicates that 805,000 Americans will face a new or recurrent myocardial infarction (MI) attack every year. Frailty, a conceptual syndrome categorized by a functional decline that occurs with aging, has been linked to adverse health outcomes in cardiovascular disease and all cardiac-related procedures in general. It is therefore reasonable to deliberate that more conservative medical therapy or medical management should be considered in the frail population when managing acute coronary syndrome. This course of action has, in fact, been documented in clinical practice. However, the recent Functional Assessment in Elderly MI Patients with Multivessel Disease trial, in which all subjects were 75 years of age or above, indicated that the more invasive complete revascularization approach may be favorable over incomplete or culprit-only revascularization in patients with acute MI. In this review, we will discuss coronary heart disease and review guidelines and procedures for culprit lesion identification, including electrocardiogram procedures, coronary angiography, intravascular ultrasound, fractional flow reserve, and instantaneous fractional flow reserve. We then discuss the concept of complete vs culprit-only/incomplete coronary revascularization and staging. Following this, we will delve into recent trials discussing complete vs culprit-only revascularization, emphasizing the insights gleaned from this latest trial within this special frailty cohort which warrants special consideration.

Is an accurate self-perceived health risk beneficial for patients to minimize prehospital delay time at onset of a ST-segment elevated myocardial infarction (STEMI)?

High risk perception (HRP) is fundamental for adequate health behavior. However, its impact on rapid access to cardiac care after the onset of acute myocardial infarction (AMI) is not known. Conflicting evidence exists about sources that promote HRP. Data on sociodemographic and clinical characteristics of 588 AMI patients who participated in the Munich Examination of Delay in Patients Experiencing Acute Myocardial Infarction (MEDEA) study were collected at the bedside. Adjusted multivariate logistic regression models identified factors associated with HRP. Only 13.4% (n = 79) of patients had afavorable HRP level. The HRP patients did not differ from those with low risk perception (LRP) in terms of sex, age, other sociodemographic features, and somatic risk factors. Among the univariate contributors to HRP were prodromal chest pain (p = 0.0004), symptom mismatch during AMI (p < 0.0001), depression (p = 0.01), and anxiety (p = 0.005). However, family history of AMI, aprevious AMI, and knowledge of AMI remained significant in the multivariate regression model. Median delay time to reach ahospital-based emergency facility after the onset of AMI was 127 min (interquartile range [IQR]: 83-43, p = 0.02) in HRP patients and 216 min (IQR: 106-721) in LRP patients. An increasing risk perception score was associated with acorresponding stepwise decline in median delay time (p > 0.004). Self-perceived AMI risk is associated in adose-response relationship with the time needed to reach coronary care emergency facilities. Recurrent AMI, family history of AMI, and sufficient knowledge of MI contribute to risk perception, whereas somatic risk factors do not.

Electrochemical detection of myoglobin using an ultrasensitive label-free sensor derived from cubic-ZIF67@Au-rGOF-NH2 composite of MOF and GOF

Markers of myocardial injury, such as myoglobin (Mb), are substances swiftly released into the peripheral bloodstream upon myocardial cell injury or altered cardiac activity. During the onset of acute myocardial infarction, patients experience a significant surge in serum Mb levels. Given this, precise detection of Mb is essential, necessitating the development of innovative assays to optimize detection capabilities. This study introduces the synthesis of a three-dimensional hierarchical nanocomposite, Cubic-ZIF67@Au-rGOF-NH2, utilizing aminated reduced graphene oxide and zeolite imidazolium ester framework-67 (ZIF67) as foundational structures. Notably, this novel material, applied in a label-free electrochemical immunosensor, presents a groundbreaking approach for detecting myocardial injury markers. Experimental outcomes revealed ZIF67 and AuNPs exhibit enhanced affinity and growth on the 3D-rGOF-NH2 matrix, thus amplifying electrical conductivity while preserving the inherent electrochemical attributes of ZIF67. As a result, the Cubic-ZIF67@Au-rGOF-NH2 label-free electrochemical immunosensor exhibited a broad detection range and high sensitivity for Mb. The derived standard curve was ΔIp = 16.67552lgC+275.245 (R = 0.993) with a detection threshold of 3.47 fg/ml. Moreover, recoveries of standards spiked into samples ranged between 96.3% and 108.7%. Importantly, the devised immunosensor retained notable selectivity against non-target proteins, proving its potential clinical utility based on exemplary sample analysis performance.

Modifiable risk factors and risk of myocardial infarction in offspring with parental disease.

Children of patients with early-onset myocardial infarction (MI) are at increased risk, but the importance of concordant versus discordant parent-offspring risk factor profiles on MI risk is largely unknown. We quantified the long-term absolute risk of MI according to shared risk factors in adulthood. We sampled data on familial predisposed offspring and their parents from the Framingham Heart Study. Early MI was defined as a history of parental MI onset before age 55 in men or 65 in women. Individuals were matched 3:1 with non-predisposed offspring. Cardiovascular risk factors included obesity, smoking, hypertension, high cholesterol, and diabetes. We estimated the absolute 20-year incidence of MI using the Aalen-Johansen estimator. At age 40, the 20-year risk of MI varied by cholesterol level (high cholesterol 25.7% [95% confidence interval 11.2%; 40.2%] vs. non-high cholesterol 3.4% [0.5; 6.4]) among predisposed individuals and this difference was greater than in controls (high cholesterol 9.3% [1.5; 17.0] vs. non-high cholesterol 2.5% [1.1; 3.8]). Similar results were observed for prevalent hypertension (26.7% [10.8; 42.5] vs. 4.0% [0.9; 7.1] in predisposed vs. 10.8% [3.2; 18.3] and 2.1% [0.8; 3.4] in controls). Among offspring without risk factors, parental risk factors carried a residual impact on 20-year MI risk in offspring (0% [0; 11.6] for 0-1 parental risk factors versus 3.3% [0; 9.8] for ≥2 parent risk factors at age 40, versus 2.9% [0; 8.4] and 8.5% [0; 19.8] at age 50 years). Children of patients with early-onset MI have low absolute risks of MI in the absence of midlife cardiovascular risk factors, especially if the parent also had a low risk factor burden prior to MI.

Impact of diabetes on short-term outcomes in patients undergoing coronary artery bypass grafting surgery in acute coronary syndrome.

Diabetes mellitus (DM) is associated with concomitant comorbidities, such as atherosclerosis and cardiovascular disease. Coronary artery bypass grafting (CABG) surgery is the optimal therapy in diabetic patients with triple vessel disease. DM is also known to be a relevant risk factor for higher morbidity and mortality in patients who underwent elective CABG procedures. Data regarding outcomes in diabetic patients in acute coronary syndrome (ACS) is heterogeneous. This study aimed to investigate the impact of DM on short-term outcomes in patients who underwent CABG surgery in ACS. A retrospective propensity score matched (PSM) analysis of 1370 patients who underwent bypass surgery for ACS between June 2011 and October 2019 was conducted. All patients were divided into two groups: non-diabetic group (n = 905) and diabetic group (n = 465). In-hospital mortality was the primary outcome. Secondary outcomes were perioperative myocardial infarction, new onset dialysis, reopening for bleeding and duration of intensive care unit (ICU) stay. A subgroup analysis of patients with insulin-dependent and non-insulin dependent DM was also performed. After performing PSM analysis, baseline characteristics and the preoperative risk profile were comparable between both groups. The proportion of patients who underwent total arterial revascularization (p = .048) with the use of both internal thoracic arteries (p < .001) was significantly higher in the non-diabetic group. The incidence of perioperative myocardial infarction (p = .048) and new onset dialysis (p = .008) was significantly higher in the diabetic group. In-hospital mortality was statistically (p = .907) comparable between the two groups. DM was associated with a higher incidence of adverse outcomes, however with comparable in-hospital mortality in patients who underwent CABG procedure for ACS.

Cardiac arrest and post-discharge mortality in patients with myocardial infarction: A large-scale nationwide registry analysis

BackgroundCardiac arrest is a serious complication of acute myocardial infarction. The implementation of contemporary approaches to acute myocardial infarction management, including urgent revascularization procedures, has led to significant improvements in short-term outcomes. However, the extent of post-discharge mortality in patients experiencing cardiac arrest during acute myocardial infarction remains uncertain. This study aimed to determine the post-discharge outcomes of patients with cardiac arrest. MethodsWe analysed data from the J-PCI OUTCOME registry, a Japanese prospectively planed, observational, multicentre, national registry of percutaneous coronary intervention involving consecutive patients from 172 institutions who underwent percutaneous coronary intervention and were discharged. Patients who underwent percutaneous coronary intervention for acute myocardial infarction between January 2017 and December 2018 and survived for 30 days were included. Mortality in patients with and without cardiac arrest from 30 days to 1 year after percutaneous coronary intervention for acute myocardial infarction was compared. ResultsOf the 26,909 patients who survived for 30 days after percutaneous coronary intervention for acute myocardial infarction, 1,567 (5.8%) had cardiac arrest at the onset of acute myocardial infarction. Patients with cardiac arrest were younger and more likely to be males than patients without cardiac arrest. The 1-year all-cause mortality was significantly higher in patients with cardiac arrest than in those without (11.9% vs. 2.8%, p < 0.001) for all age groups. Multivariable analysis showed that cardiac arrest was an independent predictor of all-cause long-term mortality (hazard ratio: 2.94; 95% confidence interval: 2.29–3.76). ConclusionsPatients with acute myocardial infarction and concomitant cardiac arrest have a worse prognosis for up to 1 year after percutaneous coronary intervention than patients without cardiac arrest.