Search Results (177)

Pressure-controlled intermittent coronary sinus occlusion (PICSO) was initially developed to salvage ischemic myocardium. However, recent evidence suggests a more profound role: reawakening embryonic molecular pathways that facilitate myocardial regeneration. This review examines the paradigm shift in PICSO’s mechanism—from its traditional focus on infarct size reduction to its emerging role as a catalyst for myocardial repair through the reactivation of embryonic signaling. Findings suggested that myocardial decay could be ameliorated beyond salvage, revealing that PICSO enhances vascular activation in the coronary venous system, thereby influencing the fate of endothelial and myocardial cells. The theorem “embryonic recall” posits that PICSO induces molecular signals reminiscent of early cardiac development, offering a novel approach to cardiac repair in myocardial jeopardy. Noncoding RNA serves as a universal signaling event, thereby supporting the hypothesis. Yet, conflicting clinical outcomes highlight the need to redefine PICSO’s objectives, optimize device settings, and realize interventional strategies. The evolution of PICSO demands a radical shift in scientific perspective. Beyond ischemic salvage, its true potential may lie in harnessing regenerative mechanisms within the failing heart. Modern cardiology must adopt this dual role, bridging mechanical intervention with molecular rejuvenation to ensure its continued viability as a therapeutic option. PICSO, like the phoenix, may yet rise anew as a transformative force in cardiovascular medicine. Full article

The pathophysiology of ST-elevated myocardial infarction (STEMI) extends beyond coronary artery occlusion to include microvascular and endothelial dysfunction, both of which critically influence outcomes. Endocan, a soluble dermatan sulfate proteoglycan secreted by endothelial cells, has emerged as a novel biomarker of endothelial activation and dysfunction. Recent studies suggest that elevated endocan levels may carry prognostic significance in patients with STEMI, particularly those undergoing percutaneous coronary intervention (PCI). A comprehensive search of PubMed, Cochrane Library, and Google Scholar was conducted to identify studies evaluating endocan as a prognostic biomarker in STEMI. Review articles, case reports, case series, and experimental studies were excluded. Seven clinical studies, comprising sample sizes ranging from 80 to 320 patients, met the inclusion criteria. Across these studies, endocan levels were analyzed in relation to established prognostic markers and clinical outcomes. Key findings demonstrated that higher endocan levels correlated with stress hyperglycemia (r = 0.21, p < 0.05), higher SYNTAX scores, and worse in-hospital outcomes. A cutoff value of 1.7 ng/mL predicted STEMI with 76.1% sensitivity and 73.6% specificity. Elevated endocan levels also showed positive correlations with the TIMI risk score, major adverse cardiovascular events (MACE), and were identified as independent predictors of incomplete ST-segment resolution (STR) (p = 0.044) and no-reflow phenomenon (NRP) (p < 0.001, OR = 2.39, 95% CI = 1.37–4.15). Collectively, the evidence indicates that endocan is strongly associated with endothelial dysfunction, MACE, NRP post-PCI, and impaired reperfusion. Moreover, traditional prognostic indices such as TIMI and SYNTAX scores appear to correlate with circulating endocan levels. However, variability in reported cutoff values across studies highlights the need for larger, multicenter trials with standardized endpoints to establish endocan’s diagnostic and prognostic utility in STEMI. Full article

Acute extracardiac conditions can occasionally produce electrocardiographic abnormalities that closely mimic acute coronary occlusion, posing a diagnostic challenge and increasing the risk of unnecessary activation of invasive cardiac pathways. Severe gastrointestinal distension, although uncommon, is a recognized cause of transient ST-segment elevation due to mechanical displacement of the heart, autonomic imbalance, and abrupt changes in ventricular loading conditions. These alterations may be particularly misleading in patients with chronic regional wall motion abnormalities, in whom new ECG changes risk being misinterpreted as recurrent ischemia. We report the case of a 68-year-old man with a history of inferior myocardial infarction who presented with marked abdominal distension secondary to a closed-loop small bowel obstruction. Despite the absence of chest pain, his ECG showed significant anterolateral ST-segment elevation. High-sensitivity troponin I remained negative, and transthoracic echocardiography demonstrated preserved anterior and apical motion, chronic inferior akinesia, and unchanged global longitudinal strain. Following nasogastric decompression, the ST-segment normalized completely within fifteen minutes. Subsequent imaging confirmed a closed-loop volvulus requiring urgent surgical intervention, with full bowel viability preserved. This case underscores the importance of integrating clinical context, biomarkers, and rapid echocardiographic assessment when evaluating ST-segment elevation, helping avoid unnecessary coronary angiography in the presence of extracardiac causes. Full article

Background: Takotsubo syndrome (TTS) often mimics anterior ST-elevation myocardial infarction (STEMI) caused by left anterior descending (LAD) occlusion, yet the two entities differ fundamentally in pathophysiology and mechanical behavior. Two-dimensional speckle-tracking echocardiography (2D-STE) enables detailed assessment of left ventricular (LV) deformation beyond conventional ejection fraction (LVEF). This meta-analysis compared global and regional LV strain patterns in TTS versus LAD-related anterior STEMI during the acute phase. Methods: A systematic search of PubMed, Embase, and Scopus through October 2025 identified observational case–control studies directly comparing TTS and angiographically confirmed anterior STEMI, with LV mechanics assessed by 2D-STE. Random-effects models were used to pool standardized mean differences (SMDs) for LVEF; global longitudinal strain (GLS); apical, mid-ventricular, and basal longitudinal strain (ALS, MLS, BLS); and global radial strain (GRS). Heterogeneity (I²), publication bias (funnel plots, Egger’s test), meta-regression, and leave-one-out sensitivity analyses were performed. Results: Six studies comprising 221 TTS and 290 anterior STEMI patients met the inclusion criteria. TTS patients were older, predominantly female, and had fewer metabolic risk factors, while LV size was comparable. LVEF was significantly lower in TTS (SMD −1.149; 95% CI −2.20 to −0.10; p = 0.032), with stable findings across sensitivity analyses and no evidence of publication bias. GLS, ALS, MLS, and BLS showed only a non-significant trend toward greater impairment in TTS, and these comparisons were limited by marked inter-study heterogeneity. In contrast, GRS was significantly and consistently more reduced in TTS (SMD −1.284; 95% CI −1.59 to −0.98; p < 0.001), indicating more profound global radial dysfunction. Meta-regression showed no significant influence of demographic factors or vendor-specific software on LVEF or GLS differences. Conclusions: Compared with LAD-related anterior STEMI, TTS is associated with more severely depressed LVEF and markedly impaired radial strain, while longitudinal strain differences remain inconclusive and suggest only a potential trend toward greater dysfunction, reflecting the limited and heterogeneous evidence. These findings are consistent with diffuse, stress-induced myocardial stunning in TTS and suggest that 2D-STE may aid differentiation between stress cardiomyopathy and ischemic infarction in the acute setting, although longitudinal strain parameters should be interpreted cautiously and regarded as hypothesis-generating. Full article

ST-segment elevation myocardial infarction (STEMI) represents a time-critical medical emergency where complete coronary artery occlusion initiates progressive myocardial necrosis. The fundamental principle of modern STEMI care—“Time is Muscle”—establishes that ischemic duration directly determines infarct size and clinical outcomes. Each minute of delay correlates with increased mortality, larger infarcts, and a higher risk of heart failure development. Total ischemic time encompasses both patient-mediated delays (often the largest component) and system-related delays, each influenced by distinct factors requiring targeted interventions. This comprehensive review analyzes the components of total ischemic time, quantifies the clinical consequences of delay, and evaluates evidence-based mitigation strategies. We examine the evolution from fibrinolysis to primary percutaneous coronary intervention and the resulting logistical challenges. System-level interventions—including public awareness campaigns, regionalized STEMI networks, pre-hospital ECG acquisition, and standardized hospital protocols—have dramatically reduced treatment times. However, persistent disparities based on geography, presentation timing, sex, race, and age remain problematic. Emerging technologies, particularly artificial intelligence for ECG interpretation, offer promise for further time reduction. Full article

Some studies report better outcomes in cell therapy for myocardial infarction (MI) with repeated administrations. We aimed to elucidate the potential differences in terms of cardiac function and protein expression after one or three doses of cardiosphere-derived cells (CDCs) in a porcine MI model. CDCs were isolated from swine cardiac explants, cultured in cardiomyocyte growth medium (CGM), and prepared for administration. Pigs surviving a 90 min balloon occlusion of the mid-left anterior descending coronary artery (LAD) were randomly allocated to receive vehicle (CON), one (D1), or three (D3) doses of 30 × 10⁶ CDCs via the infarct-related coronary artery. Cardiac function was assessed with magnetic resonance at baseline and 10 weeks. Programmed electrical stimulation to study arrhythmogenicity was performed at 10 weeks. High-throughput quantitative proteomic analysis of infarcted tissue was performed to identify biological processes based on protein abundance changes between groups. No significant differences were found between the three groups for any cardiac function parameter at 10 weeks. No increase in ventricular tachycardia inducibility was seen in treated groups. However, gene ontology and topological analyses revealed potentially beneficial molecular adaptations. Upregulation of GYS1, AGL, and GBE1 indicated an increase in glycogen biosynthesis and energy availability, while an increase in ANK2, along with hub proteins ALB and TRAP1, suggested cardioprotective effects. Furthermore, the increase in remodeling-related proteins, including EPHA4, PODN, and ALPK3, pointed to favorable structural adaptation following infarction. In conclusion, the intracoronary administration of single or repeated doses of 30 × 10⁶ CDCs to a porcine reperfused MI model shows only slight differential improvement in both cardiac function and protein profile in this experimental setting, thus presenting limited translational potential. Full article

Background/Objectives: Unlike post-mortem histopathology, cardiovascular magnetic resonance (CMR) and positron emission tomography (PET) enable longitudinal assessment of structural, functional, and metabolic alterations in preclinical myocardial infarction models. This study aims to describe the temporal evolution of infarct size and systolic function by CMR and glucose consumption via PET, explore their differences in non-reperfused and reperfusion infarction models, and assess their capacity to predict histology-derived infarct size and systolic function at chronic phase CMR. Methods: Two murine models of myocardial infarction were generated using permanent (non-reperfused, n = 8) or transient (reperfused, n = 9) coronary occlusion. CMR and fluorine-18 2-fluoro-2-deoxyglucose PET imaging were performed at baseline and at 1, 7, and 21 days post-infarction to quantify infarct size, systolic function, and myocardial glucose metabolism. Infarct size was also assessed using Masson’s trichrome staining. Results: At 24 h post-infarction, CMR-derived infarction together with significant reduction in systolic function and glucose metabolism were already noted in both models. At 21-day CMR, however, reperfused mice showed lower infarct size and more preserved systolic function compared to their non-reperfused counterparts, while no differences in glucose metabolism were reported. Infarct size and systolic function at 1-day CMR and the number of segments with reduced glucose consumption at 1-day PET independently predicted histology-derived infarct size and long-term systolic function. Conclusions: Combined PET/CMR imaging enables non-invasive, sequential evaluation of infarct size, systolic function, and glucose metabolism in experimental myocardial infarction. This multimodality approach is well suited for assessing the efficacy of emerging therapies in preclinical research. 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

Background: Thyrotoxicosis is a systemic condition with well-documented cardiovascular effects, but its role as a precipitant of acute coronary syndromes (ACS) is often overlooked. This review summarizes clinical cases and original studies from the last 20 years, describing ACS triggered by thyrotoxicosis. Methods: Following PRISMA 2020 guidelines, we searched PubMed, Scopus, and Embase for reports published between 2004–2025. Only case reports and original articles were included. Data extracted included demographics, ECG findings, angiography results, thyroid function, etiology of hyperthyroidism, and outcomes. Results: A total of 35 cases were identified. The mean age was in the fourth decade of life, with a female predominance (57%, 20 out of 35). More than half of the patients presented with ST-segment elevation myocardial infarction (STEMI) or STEMI equivalents (21 out of 35; 60%). Electrocardiographic abnormalities most often involved anterior or inferior leads. Coronary angiography revealed normal vessels or diffuse vasospasm in 18 cases (51%), while thrombotic occlusion was observed in 4 cases (11%), spontaneous dissection in 2 cases (6%), and myocardial bridging in 3 cases (9%). The leading cause of thyrotoxicosis was Graves’ disease (≈65%), followed by painless thyroiditis, iatrogenic causes, and gestational hyperthyroidism. Thyroid storm was reported in approximately 20% of cases and was associated with malignant ventricular arrhythmias or sudden cardiac death. Conclusions: Thyrotoxicosis should be recognized as a rare but important trigger of ACS, especially in young patients without traditional risk factors. Pathophysiological mechanisms include coronary vasospasm, increased myocardial oxygen demand, and hypercoagulability. Early recognition may prevent unnecessary revascularization and optimize outcomes through integrated endocrine and cardiac management. Full article

Background: Transcatheter aortic valve implantation (TAVI) is an established treatment for severe aortic stenosis in elderly and high-risk patients. However, prosthetic valve endocarditis (PVE) remains a rare but devastating complication. Its diagnosis is often delayed due to atypical clinical manifestations and the frequent occurrence of culture-negative endocarditis. Case Presentation: We report the case of a 68-year-old woman with a prior TAVI who presented with sacroiliitis, initially interpreted as a localized musculoskeletal infection. Subsequent evaluation revealed infective endocarditis involving the prosthetic aortic valve and the native mitral valve. Blood cultures remained negative, most likely due to prior antibiotic therapy, which complicated timely diagnosis. During hospitalization, the patient developed acute ST-segment elevation myocardial infarction (STEMI), caused by coronary septic embolization. Discussion: Distinguishing septic emboli from thrombotic occlusion in the setting of STEMI complicating endocarditis is extremely challenging but essential, as therapeutic approaches diverge. While percutaneous coronary intervention is the standard treatment for thrombotic occlusion, it carries major risks of septic embolization, including stent infection, mycotic aneurysm, and uncontrolled sepsis. Conclusions: This case highlights the need for high clinical suspicion of PVE in atypical presentations, the diagnostic challenges of culture-negative endocarditis, and the therapeutic dilemmas posed by acute coronary complications without clear guideline-based solutions. Full article

Background: Rituximab is a monoclonal antibody targeting CD20, commonly used to treat autoimmune diseases such as granulomatosis with polyangiitis (GPA) and rheumatoid arthritis. While generally well-tolerated, serious adverse events, including infusion reactions and infections, are well-documented. Case Summary: We report a rare case of rituximab-induced ST-elevation myocardial infarction (STEMI) in a 26-year-old woman with no cardiovascular risk factors. She developed crushing chest pain after her first 1 g rituximab infusion, with recurrent symptoms upon re-exposure. Cardiac catheterization revealed a left circumflex artery occlusion. Additional workup showed c-ANCA positivity, cryoglobulinemia, pauci-immune glomerulonephritis, and findings consistent with GPA. Rituximab was discontinued, and she was transitioned to steroids, cyclophosphamide, and leuprolide, with no further cardiac events. Discussion: This is the first reported case in a young, previously healthy woman. Clinicians should consider rituximab-associated myocardial injury, especially in autoimmune or hypercoagulable states. Take-Home Message: Remain vigilant for cardiac events during rituximab infusions in patients with inflammatory diseases. Full article

Background/Objectives: Thrombosis, a critical condition that can have severe consequences, such as myocardial infarction and cerebral infarction, can be induced by steroid drugs. Although the mechanisms for inducing thrombosis are known for some types of steroid drugs, much remains unknown about the differences in the tendency and mechanisms for thrombosis. Methods: To address this knowledge gap, we analyzed the relationship between thrombosis and steroid use by utilizing the U.S. Food and Drug Administration Adverse Event Reporting System database. From the database, we extracted demographic and drug information and information on reported adverse events from 2004 to 2024. We characterized drugs according to physiological function, receptor specificity, and Anatomic Therapeutic Chemical classification and calculated the proportion of steroid drugs that were likely to induce thrombosis. Results: Among steroid drugs, sex hormones such as androgens, progestogens, and estrogens appeared to have particularly high potential for causing thrombotic events. Results of principal component analysis and cluster analysis indicated that sex hormone preparations were associated with an increased risk of venous thrombosis. In addition, cardiovascular medications and mineralocorticoids, which are used to treat diseases of major organs, showed a tendency to induce large-vessel occlusions. Conclusions: These findings may be useful for selecting steroid drugs for patients who are at risk for similar adverse effects. Full article

Background: The STEMI/NSTEMI classification guides management and quality metrics for acute myocardial infarction (AMI). We examined whether the final cath-lab diagnosis of STEMI versus NSTEMI correlates more closely with door-to-balloon (D2B) time than with either ST-segment elevation (STE) on pre-angiogram ECG or a culprit lesion with TIMI 0-1 flow. Methods: This retrospective study analyzed 410 patients with AMI from the DOMI-ARIGATO database who underwent coronary angiography. For each patient, we recorded FDx coded by the interventional cardiologist, D2B < 120 min versus > 120 min, STE criteria (Fourth Universal Definition), and angiographic TIMI 0-1 culprit. Predictors of FDx-STE discordance were evaluated with multivariable logistic regression. Results: Among 410 angiographed AMI patients (mean age 63 ± 13; 71% male), 165 (40.2%) received an FDx-STEMI and 245 (59.8%) an FDx-NSTEMI. D2B time showed 94% agreement with FDx (160/165 FDx-STEMI treated < 120 min; 225/245 FDx-NSTEMI treated > 120 min), exceeding concordance for STE (82%; p < 0.001) and TIMI 0-1 flow (75%; p < 0.001). FDx and STE diverged in 75 patients (18%): 60 rapidly treated STE-negative cases were labelled STEMI, whereas 15 delayed STE-positive cases were labelled NSTEMI. In regression analysis, D2B < 120 min remained the sole independent predictor of discordance (adjusted OR 6.7, 95% CI 3.5–13.8). Conclusions: In this registry, the cath-lab label “STEMI” showed the strongest correlation with meeting a 120 min benchmark, exceeding correlations for STE or angiographic occlusion. These findings suggest that quality-metric compliance, rather than electrocardiographic or anatomic criteria, predominantly drives final diagnosis. Full article

Although cardiac metabolic adaptation has been observed in response to the ischemia–reperfusion, the specific temporal and spatial changes occurring in the main regulators of myocardial glucolipid metabolism in the infarcted heart have not been fully characterized. Myocardial infarction (MI) was induced in female swine by transient coronary occlusion. The study design consisted of one control and four MI groups (no reperfusion, 1 min, 1 week, and 1 month after reperfusion). Metabolites obtained from the coronary sinus were determined at baseline, during ischemia, and after coronary reperfusion. mRNA expression of genes related to beta-oxidation and glucose transport were quantified in the five experimental groups and in three myocardial regions (infarcted, adjacent, and remote). In the coronary sinus, reduced glucose and increased lactate levels were detected during ischemia and soon after reperfusion. However, non-esterified fatty acids increased during reperfusion. A general upregulation of genes implicated in glycolysis and beta-oxidation occurred during ischemia and few minutes after reperfusion. Contrarily, heightened mRNA expression of glucose transporters and decay in regulators of beta-oxidation were observed one week after coronary reperfusion. Glycolysis and beta-oxidation are activated during ischemia and few minutes after coronary reopening, while a shift from beta-oxidation to glycolysis is evidenced a few days afterwards. Full article

A 62-year-old man presented with ST-elevation myocardial infarction and advanced tophaceous gout, despite long-term urate-lowering therapy. His history included chronic kidney disease, hypertension, heart failure, and atrial fibrillation. Examination revealed severe joint deformities with multiple tophi. Coronary angiography showed multivessel disease with critical right coronary artery stenosis, treated with primary percutaneous coronary intervention. Following a Heart Team consultation, the patient was bridged with cangrelor and underwent urgent hybrid coronary artery bypass grafting and left atrial appendage occlusion. This case highlights the systemic burden of treatment-refractory gout, with progressive cardiovascular and renal complications. Tophaceous gout represents a distinct, high-risk phenotype associated with increased mortality and reduced quality of life. Despite standard therapies, this patient experienced continued disease progression, prompting referral for advanced treatment with pegloticase and canakinumab. Multidisciplinary care and personalized strategies are essential in managing severe, refractory gout with multi-organ involvement. Full article