Search Results (103)

Background and Objectives: Coronary heart disease is a leading cause of death in developed countries. While ECG-gated coronary CT is commonly used to detect coronary artery stenosis, the potential of non-ECG-gated CT (NECE-CT) to reveal incidental myocardial perfusion defects indicative of acute myocardial infarction (AMI) remains underexplored, particularly in emergency settings where rapid diagnosis is crucial. Materials and Methods: We retrospectively analyzed 22 suspected AMI patients from the emergency department who underwent NECE-CT without either an initial AMI diagnosis or available cardiac enzyme or ECG data. Results: AMI was confirmed in 45% (n = 10) of patients, with 30% (n = 3/10) showing elevated troponin I levels only after the CT exam. In the AMI group, all patients had perfusion defects, with 20% (n = 2) showing transmural defects and 80% (n = 8) showing endocardial defects. In contrast, all patients in the non-AMI group exhibited endocardial defects. Coronary artery calcification was significantly higher in the AMI group (70%) compared to the non-AMI group (25%, p < 0.05). Conclusions: These findings suggest that NECE-CT may reveal myocardial perfusion defects as an ancillary sign of AMI. While not a standalone diagnostic tool, careful evaluation of the myocardium in emergency CT scans may raise suspicion of AMI in patients with atypical presentations, offering more insight than standard methods. Further prospective studies with larger cohorts are needed to validate the clinical utility of these incidental findings. Full article

Acute myocardial infarction (AMI) is a significant factor leading to the death of patients with coronary heart disease. Both AMI and reperfusion therapy after AMI cause myocardial cell death, which plays a significant role in heart failure. Following the restoration of blood flow during reperfusion, myocardial cells generate a large amount of oxygen free radicals, causing various forms of myocardial ischemia–reperfusion (IR) injury (IRI), ultimately leading to multiple types of myocardial cell death, among which apoptosis and necroptosis are the two major types. Given the extremely limited regenerative capacity of myocardium, inhibiting myocardial cell apoptosis and necroptosis is a key strategy for reducing mortality in patients with AMI. Both apoptosis and necroptosis are regulated by the BCL2 family of proteins, which were modulated by multiple signaling pathways, converging at BAK/BAX-mediated mitochondrial outer membrane permeabilization (MOMP), as well as mitochondrial inner membrane permeabilization (MIMP). BAK/BAX double knock out (DKO) mice showed reduced cell apoptosis, necroptosis, and infarct size in AMI animal models compared to wild type. This review describes the role of BCL2 family proteins in regulating apoptotic and necroptotic myocardial cell death during AMI and IR, explores the upstream pathways modulating apoptosis and necroptosis, and summarizes the recent advances in targeting BAK and/or BAX for cardiac protection. In addition, targeted delivery of BAK/BAX inhibitors to cardiomyocytes during AMI or myocardial IR has the potential to reduce myocardial cell death and therefore lower the mortality and enhance long-term prognosis for myocardial infarction patients. Full article

Acute myocardial infarction is the most common form of coronary artery disease, and myocardial ischemia–reperfusion injury remains a major challenge despite advances in reperfusion therapy. Endotoxin preconditioning has been linked to reduced ischemia–reperfusion injury, but mechanisms remain unclear, and prior studies have used varied assessment methods with inconsistent results. In this study, we confirmed the protective effect of endotoxin preconditioning and assessed its role in preserving mitochondrial respiration using a multi-model approach of in vivo ischemia–reperfusion rat model, ex vivo normothermic rat heart perfusion, and in vitro hypoxia–reoxygenation in neonatal rat cardiomyocytes. Hemodynamic and cell-based analyses were performed in control (n = 5), ischemia–reperfusion/hypoxia–reoxygenation (n = 4/3), and endotoxin-pretreated (n = 5/3) groups. Low-dose endotoxin pretreatment significantly preserved left ventricular function, myocardial oxygen consumption, and mitochondrial respiration (p < 0.001). Preservation of function was associated with reduced hypoxia-inducible factor 1-alpha (HIF-1α) expression and decreased mitochondrial superoxide production, indicating reduced oxidative stress. Nonlethal endotoxin pretreatment protects the myocardium from ischemia–reperfusion injury by sustaining mitochondrial respiration and limiting oxidative damage. These findings support further investigation in large animal models to better replicate human myocardial infarction and evaluate translational potential. Full article

Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic cause of acute coronary syndrome, characterized by the development of a false lumen within the coronary arterial wall, leading to narrowing or complete occlusion of the true lumen. This underrecognized condition accounts for a substantial proportion of sudden cardiac death (SCD), particularly among young, otherwise healthy women. Macroscopically, SCAD is defined by intramural hematoma and focal thickening of the arterial wall, while histological examination demonstrates separation of the tunica media, elastic fiber degeneration, and variable inflammatory infiltrates. Proposed pathogenic mechanisms include primary intimal tear and primary intramural hematoma, frequently associated with predisposing conditions such as fibromuscular dysplasia, connective tissue disorders, and specific hormonal states. In cases of myocardial infarction, the myocardium exhibits acute ischemic necrosis and early hypoperfusion injury. Postmortem diagnosis requires meticulous coronary dissection, adjunctive histochemical and immunohistochemical staining, and, when indicated, molecular autopsy (MA). The purpose of this review is to provide an updated synthesis of current knowledge on SCAD as a cause of SCD, integrating pathogenetic, morphological, and genetic perspectives, and to emphasize the role of MA as both a diagnostic and preventive tool. Full article

Sports-associated traumatic brain injury is emerging as an under-recognized driver of acute and chronic cardiovascular diseases. Larger population-based studies show that individuals with moderate-to-severe traumatic brain injury experience up to a two-fold excess risk of incident hypertension, coronary artery disease, myocardial infarction, and stroke that persists for at least a decade. Among former professional American-style football players, a higher lifetime concussion burden is uniquely related to a more atherogenic cardiometabolic profile and greater long-term stroke risk. Mechanistically, an acute “sympathetic storm” triggered by cerebral injury provokes catecholamine surges, endothelial dysfunction, and myocardial stunning, manifesting as neurogenic stunned myocardium or Takotsubo-like cardiomyopathy and malignant arrhythmias. Sub-acute to chronic phases are characterized by persistent autonomic imbalance, reflected by reduced heart-rate variability and impaired baroreflex sensitivity weeks to months after concussion, coupled with neuroinflammation, hypothalamic–pituitary–adrenal axis dysregulation, and lifestyle changes that accelerate atherosclerosis. The interplay of these pathways accounts for the elevated burden of cardiovascular disease observed long after neurological function has been restored. Despite robust evidence linking TBI to adverse cardiac outcomes, contemporary sports–cardiology risk stratification prioritizes hemodynamic load, genetics, and performance-enhancing substances, largely overlooking brain injury history. This review integrates epidemiological, clinical, and mechanistic data to (i) delineate acute neurocardiac complications secondary of sports-related traumatic brain injury, (ii) synthesize evidence for chronic cardiovascular risk, (iii) highlight emerging autonomic and inflammatory biomarkers, and (iv) propose surveillance and therapeutic strategies, ranging from heart-rate-variability-guided return-to-play decisions to aggressive cardiometabolic risk modification aiming to mitigate long-term morbidity in this athletic population. By framing sports-related traumatic brain injury as a modifiable cardiovascular risk factor, we aim to foster interdisciplinary collaboration among neurologists, cardiologists, and sports medicine practitioners, ultimately improving both neurological and cardiovascular outcomes across the athlete’s lifespan. Full article

Cardiac magnetic resonance (CMR) imaging has become a key tool in evaluating myocardial injury secondary to coronary artery disease (CAD), providing detailed assessments of cardiac morphology, function, and tissue composition. The integration of artificial intelligence (AI), including machine learning and deep learning techniques, has enhanced the diagnostic capabilities of CMR by automating segmentation, improving image interpretation, and accelerating clinical workflows. Radiomics, through the extraction of quantitative imaging features, complements AI by revealing sub-visual patterns relevant to disease characterization. This systematic review analyzed AI applications in CMR for CAD. A structured search was conducted in MEDLINE, Web of Science, and Scopus up to 17 March 2025, following PRISMA guidelines and quality-assessed with the CLAIM checklist. A total of 106 studies were included: 46 on classification, 19 using radiomics, and 41 on segmentation. AI models were used to classify CAD vs. controls, predict major adverse cardiovascular events (MACE), arrhythmias, and post-infarction remodeling. Radiomics enabled differentiation of acute vs. chronic infarction and prediction of microvascular obstruction, sometimes from non-contrast CMR. Segmentation achieved high performance for myocardium (DSC up to 0.95), but scar and edema delineation were more challenging. Reported performance was moderate-to-high across tasks (classification AUC = 0.66–1.00; segmentation DSC = 0.43–0.97; radiomics AUC = 0.57–0.99). Despite promising results, limitations included small or overlapping datasets. In conclusion, AI and radiomics offer substantial potential to support diagnosis and prognosis of CAD through advanced CMR image analysis. Full article

Background/Objectives: Left ventricular (LV) pseudoaneurysm is a rare but life-threatening complication after acute myocardial infarction, often resulting from inadequate excision of damaged myocardium and use of only a xenopericardial patch during primary LV free wall rupture repair. Methods: A 62-year-old female developed a giant LV pseudoaneurysm one year after initial surgical repair of a free wall rupture with a xenopericardial patch. Imaging confirmed a large pseudoaneurysm with a broad neck and mural thrombus. She underwent pseudoaneurysmectomy, LV reconstruction with a Dacron patch overlaid by a xenopericardial patch, and concomitant mitral and tricuspid valve repair. Results: Surgical exploration revealed a broad-necked pseudoaneurysm and dehisced patch material. The aneurysm was resected, and the LV was reconstructed, resulting in the exclusion of the pseudoaneurysm and improvement of the shape and function. The patient recovered uneventfully and was discharged in good clinical condition with restored LV function. Conclusions: Pseudoaneurysm formation after LV free wall rupture repair is often due to insufficient resection and the use of only a xenopericardial patch. Surgical management with complete excision, Dacron patch reconstruction, and xenopericardial reinforcement facilitates the favorable remodeling of LV geometry and function, and reduces the risk of recurrence. Full article

Percutaneous ventricular assist devices are utilized in cases of cardiogenic shock following acute myocardial infarction (AMI). However, the mechanism underlying the beneficial effects of LV unloading in AMI remains unclear. This study aimed to examine the impact of LV unloading on cardiac function, heart failure markers, and protein degradation (autophagy and ubiquitin–proteasome system: UPS) post AMI in rats. Nine-week-old male Lewis rats were randomized into non-AMI, AMI, non-AMI with LV unloading, and AMI with LV unloading groups. LV unloading was achieved through heterotopic heart–lung transplantation. Rats were euthanized 2 and 14 days after the procedure. Cardiac functional assessment was performed using Langendorff heart perfusion. RT-PCR and Western blot analyses were conducted using the LV myocardium. The rate pressure product was comparable between the non-AMI with LV unloading group and the AMI with LV unloading at 14 days. The atrial natriuretic factor tended to be suppressed by LV unloading. LV unloading had reducing effects on the expressions of p62, selectively degraded during autophagy, both 2 and 14 days after AMI. There was no effect on the parameters for the UPS. LV unloading has a mitigating effect on the deterioration of cardiac function following AMI. Autophagy, which was suppressed by AMI, was ameliorated by LV unloading. Full article

Ischemic heart disease (IHD) is the leading cause of mortality worldwide, underscoring the urgent need for innovative therapeutic strategies. The cardiac extracellular matrix (ECM) undergoes extreme transformations during IHD, adversely influencing the heart’s structure, mechanics, and cellular signaling. Researchers investigating the regenerative capacity of the diseased heart have turned their attention to exploring the modulation of ECM to improve therapeutic outcomes. In this review, we thoroughly examine the current state of knowledge regarding the cardiac ECM and its therapeutic potential in the ischemic myocardium. We begin by providing an overview of the fundamentals of cardiac ECM, focusing on the structural, functional, and regulatory mechanisms that drive its modulation. Subsequently, we examine the ECM’s interactions within both chronically ischemic and acutely infarcted myocardium, emphasizing key ECM components and their roles in modulating angiogenesis. Finally, we discuss recent ECM-based approaches in biomedical engineering, focusing on different types of scaffolds as delivery tools and their compositions, and conclude with future directions for therapeutic research. By harnessing the potential of these emerging ECM-based therapies, we aim to contribute to the development of novel therapeutic modalities for IHD. Full article

Cardiac fibrosis is a scarring event that occurs in the myocardium in response to multiple cardiovascular disorders, such as acute myocardial infarction (AMI), ischemic cardiomyopathy, dilated cardiomyopathy, hypertensive heart disease, inflammatory heart disease, diabetic cardiomyopathy, and aortic stenosis. Fibrotic remodeling is mainly sustained by the differentiation of fibroblasts into myofibroblasts, which synthesize and secrete most of the extracellular matrix (ECM) proteins. An increase in the intracellular Ca²⁺ concentration ([Ca²⁺]_i) in cardiac fibroblasts is emerging as a critical mediator of the fibrogenic signaling cascade. Herein, we review the mechanisms that may shape intracellular Ca²⁺ signals involved in fibroblast transdifferentiation into myofibroblasts. We focus our attention on the functional interplay between inositol-1,4,5-trisphosphate (InsP₃) receptors (InsP₃Rs) and store-operated Ca²⁺ entry (SOCE). In accordance with this, InsP₃Rs and SOCE drive the Ca²⁺ response elicited by G_q-protein coupled receptors (G_qPCRs) that promote fibrotic remodeling. Then, we describe the additional mechanisms that sustain extracellular Ca²⁺ entry, including receptor-operated Ca²⁺ entry (ROCE), P2X receptors, Transient Receptor Potential (TRP) channels, and Piezo1 channels. In parallel, we discuss the pharmacological manipulation of the Ca²⁺ handling machinery as a promising approach to mitigate or reverse fibrotic remodeling in cardiac disorders. Full article

Acute myocardial infarction is an ischemic injury of the myocardium caused by an imbalance in the blood supply to myocardial tissues, which poses a serious threat to human life and health. Oxidative stress has been recognized as a significant contributor to acute myocardial infarction. Salvia miltiorrhiza Carbonisata (SMC) is among the most frequently employed herbal remedies for the treatment of acute myocardial infarction; however, the exact identity of its principal active constituents is not well defined. Research indicates that carbon dots (CDs) exhibit significant biological properties. Consequently, we initially synthesized carbon dots (CDs) from Salvia miltiorrhiza Carbonisata, with the objective of exploring how SMC-CDs mitigate isoproterenol (ISO)-induced myocardial infarction (MI) in rats. The results showed that the pretreatment with SMC-CDs markedly enhanced compromised cardiac function, mitigated myocardial fibrosis and the infiltration of inflammatory cells, decreased the size of the infarct, and suppressed cardiomyocyte apoptosis. Furthermore, the antioxidant properties of myocardial tissue were enhanced, and oxidative stress caused by free radicals was effectively mitigated by SMC-CDs, which succeeded in reducing levels of myocardial enzymes and elevating the activity of relevant ATPases. This implies that SMC-CDs could be a potential candidate for novel nanomedicine strategies designed to address cardiovascular ailments. Full article

Background/Objectives: Acute myocardial infarction (AMI) is a critical medical condition that requires immediate attention to minimise heart damage and improve survival rates. Early identification and prompt treatment are essential to save the patient’s life. Currently, the treatment strategy focuses on restoring blood flow to the myocardium as quickly as possible. However, reperfusion activates several cellular cascades that contribute to organ dysfunction, resulting in the ischaemia/reperfusion (I/R) injury. The search for treatments against AMI and I/R injury is urgent due to the shortage of effective treatments at present. In this regard, histone deacetylase (HDAC) inhibitors emerge as a promising treatment against myocardial infarction. The objective of this systematic review is to analyse the effects of HDAC inhibitors on ventricular function, cardiac remodelling and infarct size, among other parameters, focusing on the signalling pathways that may mediate these cardiovascular effects and protect against AMI. Methods: Original experimental studies examining the effects of HDAC inhibitors on AMI were included in the review using the PubMed and Scopus databases. Non-experimental papers were excluded. The SYRCLE RoB tool was used to assess risk of bias and the results were summarised in a table and presented in sections according to the type of HDAC inhibitor used. Results: A total of 18 studies were included, 10 of them using trichostatin A (TSA) as an HDAC inhibitor and concluding that the treatment improved ventricular function, reduced infarct size, and inhibited myocardial hypertrophy and remodelling after AMI. Other HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA), valproic acid (VPA), mocetinostat, givinostat, entinostat, apicidin, and RGFP966, were also analysed, showing antioxidant and anti-inflammatory effects, an improvement in cardiac function and remodelling, and a decrease in apoptosis, among other effects. Conclusions: HDAC inhibitors constitute a significant promise for the treatment of AMI due to their diverse cardioprotective effects. However, high risk of selection, performance, and detection bias in the in vivo studies means that their application in the clinical setting is still a long way off and more research is needed to better understand their benefits and possible side effects. Full article

Although coronary artery occlusion can have a negative effect on the myocardium, chronic total occlusion (CTO) exhibits different clinical features from those of acute myocardial infarction (AMI). In this study, we identify the differential associations of exosomal miRNAs with CTO and AMI. Exosomes were isolated from the plasma obtained from coronary arteries of patients undergoing percutaneous coronary intervention to treat CTO (n = 29) and AMI (n = 24), followed by small RNA sequencing, target gene predictions, and functional enrichment analyses. Promising miRNA markers were validated using real-time PCR in 35 CTO, 35 AMI, and 10 normal subjects. A total of 205 miRNAs were detected in all subjects, and 20 and 12 miRNAs were upregulated and downregulated in CTO compared to AMI patients, respectively (|fold change| > 4, FDR q < 0.05). The target genes of miRNAs that were higher in CTO patients were associated with “regulation of cell cycle phase transition”, “cell growth”, and “apoptosis”. The target genes of miRNAs that were lower in CTO patients were enriched in terms such as “muscle cell differentiation”, “response to oxygen levels”, and “artery morphogenesis”. On qRT-PCR analysis, the expression levels of miR-9-5p and miR-127-3p were significantly different between CTO and AMI patients. The miRNA expression levels accurately distinguished CTO from AMI patients with 79% specificity and 97% sensitivity. The miRNA contents of plasma exosomes were significantly different between CTO and AMI patients. The miRNAs may play important roles in CTO and AMI. Full article

Early revascularization for patients with acute myocardial infarction (AMI) is of outmost importance in limiting infarct size and associated complications, as well as for improving long-term survival and outcomes. However, reperfusion itself may further damage the myocardium and increase the infarct size, a condition commonly recognized as myocardial reperfusion injury. Several strategies have been developed for limiting the associated with reperfusion myocardial damage, including hypothermia. Hypothermia has been shown to limit the degree of infarct size increase, when started before reperfusion, in several animal models. Systemic hypothermia, however, failed to show any benefit, due to adverse events and potentially insufficient myocardial cooling. Recently, the novel technique of intracoronary selective hypothermia is being tested, with preclinical and clinical results being of particular interest. Therefore, in this review, we will describe the pathophysiology of myocardial reperfusion injury and the cardioprotective mechanics of hypothermia, report the animal and clinical evidence in both systemic and selective hypothermia and discuss the potential future directions and clinical perspectives in the context of cardioprotection for myocardial reperfusion injury. Full article

Acute myocardial infarction still represents the major cause of mortality in high-income countries. Therefore, considerable efforts have been focused on the treatment of myocardial infarctions in the acute and long-term phase, with special attention being paid to reperfusion strategies and adjunctive antithrombotic therapies. In fact, despite the successful mechanical recanalization of the epicardial conduit, a substantial percentage of patients still experience poor myocardial reperfusion or acute/subacute in-stent thrombosis. Due the delayed onset of action of currently available oral antiplatelet therapies, glycoprotein (GP) IIb–IIIa inhibitors could be expected to improve clinical outcomes, especially when administrated in the early phase of the infarction, due to the larger platelet composition of fresh thrombi, the dynamic nature of early thrombi, and the larger amount of viable myocardium existing in the early, as compared to a delayed, phase. Considerable evidence has accumulated regarding the benefits from GP IIb–IIIa inhibitors on mortality, especially among high-risk patients and when administered as an upstream strategy. Therefore, based on currently available data, GP IIb–IIIa inhibitors can be considered when the drug can be administered within the first 3 h of symptom onset and among high-risk patients (e.g., those with advanced Killip class or an anterior myocardial infarction). Even though it is not universally accepted, in our opinion, this strategy should be implemented in a pre-hospital setting (in an ambulance) or as soon as possible when arriving at the hospital (at the Emergency Room or Coronary Care Unit, irrespective of whether they are in spoke or hub hospitals). A new, second-generation GP IIb–IIIa inhibitor (zalunfiban) appears to be highly suitable as a pre-hospital pharmacological facilitation strategy at the time of first medical contact due to its favourable features, including its simple subcutaneous administration, rapid onset of action (15 min), and limited time of action (with a half-life of ~1 h), which is likely to minimize the risk of bleeding. The ongoing CELEBRATE trial, including 2499 STEMI patients, may potentially provide compelling data to support the upstream treatment of STEMI patients undergoing mechanical reperfusion. In fact, although the current therapeutic target of increased rates of timely reperfusion has been achieved, the future goal in myocardial infarction treatment should be to achieve the most rapid reperfusion prior to primary percutaneous coronary intervention, thus further minimizing myocardial damage, or, in some cases, even preventing it completely, and improving survival. Full article