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Early invasive revascularization guided by moderate to severe ischemia did not improve outcomes over medical therapy alone, underlying the need to identify high-risk patients for a more effective invasive referral. CMR could determine the myocardial extent and matching locations of ischemia and infarction. This study sought to investigate if CMR peri-infarct ischemia is associated with adverse events incremental to known risk markers. Consecutive patients were included in an expanded cohort of the multicenter SPINS (Stress CMR Perfusion Imaging in the United States) study. Peri-infarct ischemia was defined by the presence of any ischemic segment neighboring an infarcted segment by late gadolinium enhancement imaging. Primary outcome events included acute myocardial infarction and cardiovascular death, whereas secondary events included any primary events, hospitalization for unstable angina, heart failure hospitalization, and late coronary artery bypass surgery. Among 3,915 patients (age: 61.0 ± 12.9 years; 54.7% male), ischemia, infarct, and peri-infarct ischemia were present in 752 (19.2%), 1,123 (28.8%), and 382 (9.8%) patients, respectively. At 5.3 years (Q1-Q3: 3.9-7.2 years) of median follow-up, primary and secondary events occurred in 406 (10.4%) and 745 (19.0%) patients, respectively. Peri-infarct ischemia was the strongest multivariable predictor for primary and secondary events (HR adjusted : 1.72 [95% CI: 1.23-2.41] and 1.71 [95% CI: 1.32-2.20], respectively; both P < 0.001), adjusted for clinical risk factors, left ventricular function, ischemia extent, and infarct size. The presence of peri-infarct ischemia portended to a >6-fold increased annualized primary event rate compared to those with no infarct and ischemia (6.5% vs 0.9%). Peri-infarct ischemia is a novel and robust prognostic marker of adverse cardiovascular events. [ABSTRACT FROM AUTHOR]

Context: Both the aging of the population and the increase in noncommunicable diseases may influence the progression and outcomes culminating in death, changing the evolution of ischemic heart diseases (IHDs) and their associated causes. Using the multiple causes of death method could help understand the magnitude of these relationships and enable better targeting of investments in health. Objectives: To evaluate the mortality from IHD in Brazil between 2006 and 2020 using the method of multiple causes and identify differences in the distribution pattern of IHD mortality by sex and geographic region. Methods: Based on information extracted from death certificates (DCs) obtained from the database of the Department of Informatics of the Unified Health System (DATASUS), we used the multiple causes method to analyze the causes of death associated with IHD when IHD was defined as the underlying cause of death (UC) and the causes of death listed as the UC when IHD was recorded in any other lines of the DC, from 2006 to 2020, in Brazil. Subsequently, the proportion of these causes of death and differences between sexes and geographic regions were evaluated, with statistical relevance analyzed using the chi-square test, and the dependence between factors illustrated using stacked bar charts and small-world network graphs. Results: When IHD was listed as the UC of death, the most frequent associated causes of death were, in descending order of frequency, acute myocardial infarction (AMI), arterial hypertension (AH), chronic ischemic heart disease (CHID), heart failure (HF), and diabetes mellitus (DM). When IHD was mentioned in any line of the DC, the most frequent UCs of death were AMI followed by DM, CIHD, chronic obstructive pulmonary disease (COPD), stroke, dyslipidemia, and, in the year 2020, COVID-19. The most frequent cause of death in women were DM as the UC and associated cause of death, AH as the UC, and CIHD and Alzheimer's disease as associated causes of death, while the most frequent causes of death in men were substance dependence as the UC and associated cause of death, and cancer as an associated cause of death. The most frequent causes of death were DM and stroke in the North and Northeast, dyslipidemia and obesity in the Midwest, Alzheimer's disease in the South and Southeast, and atherosclerotic heart disease (AHD) and COPD in the South. Conclusions: Several diseases – including AMI, AH, CIHD, HF, and DM – were the most frequent associated causes of death when IHD was recorded as the UC. In contrast, AMI, DM, CIHD, COPD, and stroke were the most frequent UCs when IHD was listed as an associated cause of death. The degree of these associations varied between sexes and geographic regions. [ABSTRACT FROM AUTHOR]

BACKGROUND: Myocardial infarction is one of the most serious cardiovascular diseases at present, and the existing clinical treatment options such as thrombolytic therapy, percutaneous coronary intervention and coronary artery bypass grafting cannot fully restore the myocardial damage caused by ischemia. Stem cell-derived exosomes for the treatment of myocardial infarction have been a hot research topic in recent years, but the low yield of natural-derived exosomes, the difficulty and time consuming nature of obtaining them, and the poor homing effect have limited their clinical application. In this context, the construction of artificial exosomes as an alternative to natural exosomes has become an effective strategy to solve the above problems. OBJECTIVE: To expound the research status of artificial exosomes in the treatment of myocardial infarction, and classify them into two design modes: semiartificial and full-artificial, and discuss the research progress and problems of the two modes, finally, make the evaluation and prospect of its clinical application in the future. METHODS: PubMed and CNKI were searched for relevant articles with “artificial exosomes, myocardial infarction, engineering” in Chinese, and “artificial exosome, hybrid exosome, myocardial infarction, nanoparticle, drug delivery system” in English. The focus of the search was from January 2017 to December 2022, and some of the classic forward literature was included. A preliminary selection was conducted through reading titles and abstracts. Repetitive studies, low-quality journals and irrelevant articles were excluded. Finally, 73 articles were included for review. RESULTS AND CONCLUSION: (1) By semi-artificially modifying exosomes, whether it is the modification of targeting peptides, hybridization of biofilms or the assistance of magnetic substances, traditional exosome therapies with insufficient targeting and low retention rate and easy to be cleared by the reticuloendothelial system have improved the efficiency of traditional exosome therapy for myocardial infarction. However, these strategies have problems such as unclear modification efficiency, medical ethics, and biotoxicity. (2) Fully artificial bionic exosomes have a higher degree of design freedom compared to exosome modification, which can solve the problems of high extraction and storage difficulties of exosomes of natural origin and limitations of large-scale production; however, this artificial exosome strategy still lacks reliable preclinical data support and biosafety testing, and has not yet formed a standardized process required for large-scale production; therefore, before applying to the clinic, the artificial exosome solution as an alternative to natural exosomes still needs continuous in-depth research by researchers. [ABSTRACT FROM AUTHOR]

Stem cells represent an attractive resource for cardiac regeneration. However, the survival and function of transplanted stem cells is poor and remains a major challenge for the development of effective therapies. As two main cell types currently under investigation in heart repair, mesenchymal stromal cells (MSCs) indirectly support endogenous regenerative capacities after transplantation, while induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) functionally integrate into the damaged myocardium and directly contribute to the restoration of its pump function. These two cell types are exposed to a common microenvironment with many stressors in ischemic heart tissue. This review summarizes the research progress on the mechanisms and challenges of MSCs and iPSC-CMs in post-MI heart repair, introduces several randomized clinical trials with 3D-mapping-guided cell therapy, and outlines recent findings related to the factors that affect the survival and function of stem cells. We also discuss the future directions for optimization such as biomaterial utilization, cell combinations, and intravenous injection of engineered nucleus-free MSCs. • IPSC-CMs and MSCs have emerged as the most promising options for ischemic myocardial repair. • The survival and function of transplanted stem cells is poor and remains a major challenge for the development of effective therapies. • Three stress conditions affect the survival and function of stem cells in the ischemic heart: low oxygen/nutrients, metabolic disorders, and inflammation. • Future studies may focus on the selection of patients, the optimization of stem cells, the combination of cells with biomaterials, and repeated intravenous delivery. [ABSTRACT FROM AUTHOR]

Background: Acute Coronary Syndrome (ACS), with or without ST-segment elevation, is a major contributor to global mortality and morbidity. Swift diagnosis and treatment are vital for mitigating cardiac damage and improving long-term outcomes. The 12-lead electrocardiogram (ECG) currently serves as the gold standard for diagnosis in ACS with ST-segment elevation and may support the diagnosis in ACS without ST-segment elevation. However, the growing prevalence of smartwatches enables the acquisition of electrocardiographic data without traditional ECG equipment. While smaller studies support smartwatch ECG use, larger-scale validation within ACS remains lacking. The ACS WATCH II study aims to validate smartwatch ECG recordings for ACS. Methods: The primary objective is to validate smartwatch-obtained electrocardiographic data in patients presenting with ACS. Two cohorts of 120 patients each, presenting ACS with and without ST-segment elevation, will be assessed. Smartwatches will capture recordings of leads I, III, and V2 alongside standard ECGs. These leads, chosen due to a 97% ACS diagnosis sensitivity in previous studies, will undergo blind evaluation by two experienced external assessors against conventional ECG. Additionally, a control sample of 60 healthy individuals will be included. Conclusions: ACS WATCH II pioneers large-scale prospective validation of smartwatch ECG recordings in ACS patients. Additionally, it indirectly validates a swift diagnostic approach using three leads (I, III, and V2). This could expedite time-critical ACS diagnoses and simplify access through smartwatch-based diagnosis. [ABSTRACT FROM AUTHOR]

With cardiovascular disease (CVD) being a primary source of global morbidity and mortality, it is crucial that we understand the molecular pathophysiological mechanisms at play. Recently, numerous pro-inflammatory cytokines have been linked to several different CVDs, which are now often considered an adversely pro-inflammatory state. These cytokines most notably include interleukin-6 (IL-6),tumor necrosis factor (TNF)α, and the interleukin-1 (IL-1) family, amongst others. Not only does inflammation have intricate and complex interactions with pathophysiological processes such as oxidative stress and calcium mishandling, but it also plays a role in the balance between tissue repair and destruction. In this regard, pre-clinical and clinical evidence has clearly demonstrated the involvement and dynamic nature of pro-inflammatory cytokines in many heart conditions; however, the clinical utility of the findings so far remains unclear. Whether these cytokines can serve as markers or risk predictors of disease states or act as potential therapeutic targets, further extensive research is needed to fully understand the complex network of interactions that these molecules encompass in the context of heart disease. This review will highlight the significant advances in our understanding of the contributions of pro-inflammatory cytokines in CVDs, including ischemic heart disease (atherosclerosis, thrombosis, acute myocardial infarction, and ischemia-reperfusion injury), cardiac remodeling (hypertension, cardiac hypertrophy, cardiac fibrosis, cardiac apoptosis, and heart failure), different cardiomyopathies as well as ventricular arrhythmias and atrial fibrillation. In addition, this article is focused on discussing the shortcomings in both pathological and therapeutic aspects of pro-inflammatory cytokines in CVD that still need to be addressed by future studies. [ABSTRACT FROM AUTHOR]

Ischemic heart disease (IHD) is a condition where the heart muscle does not receive enough blood flow, leading to cardiac dysfunction. Restoring blood flow to the coronary artery is an effective clinical therapy for myocardial ischemia. This strategy helps lower the size of the myocardial infarction and improves the prognosis of patients. Nevertheless, if the disrupted blood flow to the heart muscle is restored within a specific timeframe, it leads to more severe harm to the previously deprived heart tissue. This condition is referred to as myocardial ischemia/reperfusion injury (MIRI). Until now, there is a dearth of efficacious strategies to prevent and manage MIRI. Hormones are specialized substances that are produced directly into the circulation by endocrine organs or tissues in humans and animals, and they have particular effects on the body. Hormonal medications utilize human or animal hormones as their active components, encompassing sex hormones, adrenaline medications, thyroid hormone medications, and others. While several studies have examined the preventive properties of different endocrine hormones, such as estrogen and hormone analogs, on myocardial injury caused by ischemia-reperfusion, there are other hormone analogs whose mechanisms of action remain unexplained and whose safety cannot be assured. The current study is on hormones and hormone medications, elucidating the mechanism of hormone pharmaceuticals and emphasizing the cardioprotective effects of different endocrine hormones. It aims to provide guidance for the therapeutic use of drugs and offer direction for the examination of MIRI in clinical therapy. [Display omitted] [ABSTRACT FROM AUTHOR]

The incidence and outcomes of high bleeding risk (HBR) patients in a community cohort according to the Academic Research Consortium (ARC) criteria is not known. We hypothesized that HBR is common and associated with worse outcomes for all-comers with myocardial infarction. We prospectively collected all patients with cardiac troponin T > 99th percentile upper limit of normal (≥0.01 ng/mL) in Olmsted County between 2003 and 2012. Events were retrospectively classified as type 1 myocardial infarction (T1MI), type 2 myocardial infarction (T2MI), or myocardial injury. Patients were further classified as HBR based on the "ARC-HBR definition." Outcomes included all-cause mortality, cardiovascular mortality, recurrent MI, stroke, and major bleeding. 2419 patients were included in the final study; 1365 were classified as T1MI and 1054 as T2MI. Patients were followed for a median of 5.5 years. ARC-HBR was more common in T2MI than T1MI (73% vs 46%, p < 0.001). Among patients with T1MI, HBR was associated with higher all-cause mortality (HR 3.7, 95% CI 3.2–4.5, p < 0.001), cardiovascular mortality (4.7, 3.6–6.3, p < 0.001), recurrent MI (2.1, 1.6–2.7, p < 0.001), stroke (4.9, 2.9–8.4, p < 0.001), and major bleeding (6.5, 3.7–11.4, p < 0.001). For T2MI, HBR was similarly associated with higher all-cause mortality (HR 2.1, 95% CI 1.8–2.5, p < 0.001), cardiovascular mortality (2.7, 1.8–4.0, p < 0.001), recurrent MI (1.7, 1.1–2.6, p = 0.02) and major bleeding (HR 15.6, 3.8–63.8, p < 0.001). HBR is common among unselected patients with T1MI and T2MI and is associated with increased overall and cardiovascular mortality, recurrent cardiovascular events, and major bleeding on long-term follow up. • Approximately 75% of patients with type 2 myocardial infarction and 50% of patients with type 1 myocardial infarction are at high bleeding risk. • High bleeding risk is associated with elevated cardiac mortality, recurrent myocardial infarction, stroke, and major bleeding over 6 years. • All-cause mortality is high among patients with high bleeding risk, with >50% of those with type 1 and >75% with type 2 myocardial infarction deceased over 6 years. [ABSTRACT FROM AUTHOR]

Lack of physical activity (PA) and sarcopenia is a known risk factors for ischemic heart disease (IHD). However, considering their coexistence in the middle-aged and elderly population, the interaction of these two factors remains uncertain. Here, we investigated the interactive effects of PA and sarcopenia on IHD. We extracted 344,688 participants free of IHD at baseline from the UK Biobank. PA was classified into low, moderate, and high according to the International Physical Activity Questionnaire. Sarcopenia was identified in accordance with the European Working Group on Sarcopenia in Older People 2. Cox proportional hazard models were applied to estimate the effect of PA and sarcopenia on incident IHD and its subtypes. We also used objective PA data measured by wrist-worn devices to repeat these analyses. Over a median follow-up of 11.7 years, 24,809 (7.2%) participants developed incident IHD. Lack of PA was associated with a higher risk of IHD after adjusting for potential confounders. The hazard ratio (HR) was 1.09 (95% CI: 1.05–1.13) for individuals without sarcopenia and 1.29 (95% CI: 1.17–1.42) for those with sarcopenia. Regarding the joint effect, the combination of low PA and sarcopenia was associated with the highest risk of IHD, with an HR of 1.54 (95% CI: 1.44–1.66), and both additive and multiplicative interactions were significant (RERI 0.27, 95% CI: 0.14–0.39, p -interaction <0.01). For subtypes of IHD, the interaction was pronounced in acute myocardial infarction and chronic ischemic heart disease. These results suggest a synergistic interaction between lack of PA and sarcopenia on the risk of IHD. Findings from this study may help facilitate more effective primary prevention of IHD. [Display omitted] • Lack of physical activity (PA) and sarcopenia have synergistic interaction on ischemic heart disease (IHD). • The synergistic interaction is also found in subtypes of IHD. • Moderate volume of PA can provide beneficial protective effects. • Protective effects may only be achieved with moderate to high-intensity PA. [ABSTRACT FROM AUTHOR]