搜索结果：Cardiac failure review

Extracorporeal life support provides temporary cardiorespiratory support for patients with severe, potentially reversible cardiac and/or respiratory failure refractory to conventional measures. Its application has broadened across a wide spectrum of critical illness, yet the mechanistic basis of its physiological benefit remains incompletely defined.This review explores the mechanisms through which extracorporeal life support may confer benefit in respiratory and cardiac failure. These include restoration of gas exchange, optimization of circulatory dynamics, and mitigation of secondary organ injuries, creating conditions that facilitate tissue repair, enable adjunctive therapies, and in selected cases, provide a bridge to transplantation. In isolated respiratory failure, respiratory extracorporeal life support stabilizes gas exchange and modulates respiratory drive, enabling lung-protective ventilation and potentially attenuating ventilator- and patient self-inflicted lung injury. In cardiogenic shock, cardiac extracorporeal life support restores systemic perfusion and may reduce myocardial oxygen demand, while during cardiac arrest it may confer neuro-protective effects. In combined cardiorespiratory failure, advanced extracorporeal support modalities may augment both systemic and pulmonary circulation, supporting gas exchange and maintaining end-organ perfusion. Mechanistically, these interventions interrupt the cascade of hypoxemia- and/or hypercapnia- induced pulmonary vasoconstriction, right ventricular overload, and systemic hypoperfusion, facilitating multi-organ recovery. Optimizing patient selection, timing for extracorporeal life support initiation, and use of adjunctive therapies require a nuanced understanding of the interplay between these physiological pathways alongside careful considerations of key limitations including device-related complications, hematologic and inflammatory perturbations, and physiological trade-offs. This concise clinical review synthesizes the current literature on the mechanistic basis of extracorporeal life support in adults.

Acute coronary syndrome (ACS) is a global cause of mortality and morbidity, specifically among type 2 diabetes mellitus (T2DM) patients. Patients with hyperglycemia had unfavorable outcomes after acute myocardial infarction (AMI), with a high rate of mortality ranging between 1.5 and 2.5 fold, along with a high incidence of major adverse cardiovascular events (MACEs), compared to normoglycemic patients. Acute hyperglycemia and chronic glycemic exposure are indicated by HbA1c and are related to poor cardiovascular outcomes, which were followed by ACS. The review assessed the current evidence on the effect of the glycemic status and the strategies to control the glycemic level among T2DM patients presenting with ACS. This was a systematic review that was conducted according to the PRISMA guidelines. PubMed/MEDLINE, Web of Science, and Scopus were used as search engines to get relevant studies for the review. Eligible studies included those with ACS patients, and the glycemic status was investigated in association with the clinical outcome, such as mortality and MACEs. The Newcastle-Ottawa Scale was used to assess the quality of the study. Twelve studies included 85,000 patients; the admission of hyperglycemia was strongly related to the worst outcomes after AMI. The all-cause mortality ranges from 9.0% to 25.1%, while the variation in hospital mortality ranges between 1.9% and 9.8%. Various studies have included the high risk associated with high glucose levels. Hyperglycemia was associated with a high rate of adverse cardiac events, including heart failure, cardiogenic shock, and arrhythmias. The study concluded that poor glycemic control increases the rate of mortality during admission, and the adverse cardiac events are also enhanced among type 2 diabetes patients with ACS.

This review maps the existing evidence regarding the Social Determinants of Health (SDH) on women with heart failure (HF) in Europe, focusing on healthcare access, diagnostic pathways, clinical management and outcomes. This review followed the Joanna Briggs Institute (JBI) methodology for scoping reviews. A systematic search of six electronic databases in September 2025 yielded 3728 articles. Articles were eligible for inclusion if they featured women (aged ≥18 years) with a diagnosis of HF, were conducted in countries within the WHO-defined European Region, and specifically examined the impacts of SDH on this population. Following a two-stage screening process, 30 papers met the inclusion criteria. Data synthesis and reporting were guided by the PAGER framework (Patterns, Advances, Gaps, Evidence, and Recommendations). Nine dominant patterns were identified, centred largely on socioeconomic status, gender disparities in clinical care, and the impact of gendered labour expectations on health-seeking behaviour. These determinants significantly delay HF diagnosis and affect treatment optimisation among European women. However, a critical gap remains in sex- and age-disaggregated data with European HF datasets and research. Evidence for practice highlights the need for equity-focused care that incorporates social context into clinical management, while research recommendations prioritise investigating the underlying mechanisms behind the SDH-HF relationship to develop targeted interventions. Social determinants are fundamental drivers of heart failure outcomes for women in Europe. Addressing the intersection of structural socioeconomic barriers and clinical management is essential to mitigating health disparities and achieving care equity and outcomes for women living with HF.

Cardiac amyloidosis (CA) is an under-recognized cause of heart failure. Its prevalence in screening studies, and the extent to which selective confirmatory testing affects prevalence estimates, remain uncertain across clinical settings. We systematically searched PubMed/MEDLINE and EMBASE up to 10 August 2025. Two reviewers independently screened studies and extracted data. We grouped studies by clinical setting and combined prevalence estimates using random-effects meta-analysis. For each study, we calculated CA prevalence in 1) the whole enrolled cohort and 2) the subgroup who underwent confirmatory testing. Eighty-three studies were included. Pooled CA prevalence (whole cohort; tested subgroup) was highest in left ventricular hypertrophy/hypertrophic cardiomyopathy [LVH/HCM] (15.1%; 35.4%), followed by heart failure [HF]-mainly HF with preserved or mildly reduced ejection fraction (HFpEF/HFmrEF)-(12.6%; 13.6%) and aortic stenosis [AS] (9.6%; 11.6%). Orthopedic cohorts were lower overall (4.1%) but higher in tested subgroups (12.4%); "no specific red flags" showed 1.8% vs. 7.8%; non-cardiac bone scintigraphy was 0.49% in both denominators. Across settings, transthyretin CA predominated over light-chain CA. Several studies approached systematic screening in the general elderly; however, they were few and still applied referral criteria to second-level examinations. This meta-analysis shows that CA is relatively frequent in HFpEF/HFmrEF, severe AS, and LVH/HCM. To obtain reliable population estimates, future studies should test either all eligible participants or a predefined random sample, rather than only those with suspected disease. In clinical practice, screening strategies should clearly define which higher-risk individuals are referred for second-level tests, balancing diagnostic yield with feasibility.

There is a large spectrum of acute decompensated heart failure presentations resulting from the interaction between an acute precipitant and the patient's underlying cardiac and non-cardiac conditions. A robust classification scheme at admission is crucial for appropriate triage and targeted treatment of high-risk populations. Such a scheme should incorporate timely actionable items to generate immediate management decisions, including characteristics that suggest life-threatening clinical presentations, the factors that could be favourably modified by in-hospital interventions, such as correctable aetiologies and congestion/hypoperfusion status, and in-hospital trajectories determined by patient responses to inpatient treatment. In-hospital trajectories determine the intensity of escalation therapies and timing for initiation/up-titration of guideline-directed medical treatment. In the long term, some patients experience a progressive downsloping course culminating in advanced heart failure, while others maintain a relatively stable remitting-relapsing trajectory. For future clinical trials, a comprehensive classification scheme integrating in-hospital and long-term trajectories could profoundly affect study design by ensuring interventions are tested in more homogeneous patient populations and facilitating nuanced patient stratification.

Conduction system pacing (CSP) has emerged as a physiological alternative to biventricular pacing (BVP) for cardiac resynchronization therapy (CRT) in patients with heart failure (HF) with reduced ejection fraction (HFrEF). This systematic review and meta-analysis aimed to comprehensively compare the clinical efficacy and safety of these two strategies using the most up-to-date evidence. PubMed, Embase, Web of Science, and Cochrane Library were systematically searched up to March 2026 for randomized controlled trials (RCTs) and observational studies comparing CSP with BVP in adult HF patients (LVEF ≤ 50%). Primary outcomes included changes in LVEF, NYHA class, QRS duration, HF hospitalization (HFH), and all-cause mortality (ACM). Secondary outcomes included echocardiographic response, procedural parameters, and complications. Random-effects models were used. Heterogeneity was assessed using the I2 statistic. Publication bias was assessed using funnel plots, Egger's test, and trim-and-fill analysis. Certainty of evidence was appraised using the GRADE framework. 35 studies (10 RCTs, 25 observational; N = 7,019) were included. Compared with BVP, CSP was associated with greater improvement in LVEF (MD: 4.22%, 95%CI: 2.74%-5.70%; I2 = 72%), NYHA class (MD: -0.34, 95%CI: -0.47 to -0.21; I2 = 30%), and QRS narrowing (MD: -19.60 ms, 95%CI: -24.18 to -15.02 ms; I2 = 83%). CSP significantly reduced HFH risk (RR: 0.65, 95%CI: 0.49-0.87; I2 = 50%) and echocardiographic non-response (RR: 0.58, 95%CI: 0.41-0.82; I2 = 70%), while increasing super-response (RR: 1.86, 95%CI: 1.43-2.43; I2 = 34%). ACM was comparable between groups (RR: 0.87, 95%CI: 0.62-1.22). CSP was associated with shorter fluoroscopy time (MD: -5.04 min, 95%CI: -8.62 to -1.45 min), with similar complication rates. Benefits were most pronounced in patients with classical CRT indications (LVEF ≤ 35% with LBBB) and confirmed conduction system capture. Publication bias was detected for LVEF; trim-and-fill analysis confirmed directional benefit (adjusted MD: 2.14%). GRADE assessment demonstrated low to very low certainty of evidence. CSP may be associated with superior echocardiographic and electrocardiographic outcomes compared with BVP, but the overall certainty of the evidence remains low to very low. These findings should be considered hypothesis-generating and highlight the urgent need for large-scale, adequately powered RCTs to validate the potential benefits of CSP before its widespread adoption in routine clinical practice. https://www.crd.york.ac.uk/PROSPERO/view/CRD420251074973, identifier CRD420251074973.

Aluminum phosphide is a pesticide and rodenticide widely used in grain storage and pest management and is associated with high mortality due to refractory shock and multiorgan failure. Although severe cardiogenic shock requiring mechanical circulatory support has been predominantly reported following oral exposure, profound cardiac involvement after inhalational exposure is exceedingly rare. We report the case of a previously healthy 2-year-old girl who developed fulminant cardiogenic shock and malignant ventricular arrhythmias after inhalation of aluminum phosphide. Despite aggressive medical therapy, she experienced recurrent cardiac arrest within the first hours of hospitalization. Transthoracic echocardiography demonstrated severe left ventricular dysfunction, prompting emergent initiation of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) within the first 4 h. Multimodal extracorporeal supportive therapies, including continuous renal replacement therapy, therapeutic plasma exchange, and red blood cell exchange, were used as adjunctive measures to manage multiorgan failure. Cardiac function progressively recovered, and the patient was successfully weaned from VA-ECMO on day 11. However, she subsequently developed acute respiratory distress syndrome and suffered cardiac arrest on day 21 following progressive respiratory deterioration. The exact cause of the terminal cardiac arrest could not be determined. While adjunctive extracorporeal therapies may contribute to metabolic stabilization and organ support, this case underscores that early recognition of toxin-induced cardiac failure and timely initiation of veno-arterial extracorporeal membrane oxygenation is essential for initial stabilization in severe aluminum phosphide poisoning.

Cardiac aging is a fundamental contributor to heart failure, arrhythmias, impaired stress tolerance, and reduced cardiovascular resilience in the elderly. While intrinsic myocardial aging has been widely examined, the systemic mechanisms driving age-related cardiac decline are not fully understood. Circulating extracellular vesicles (EVs) have emerged as key mediators of intercellular and inter-organ communication, transferring proteins, lipids, and nucleic acids that modify the phenotypes of recipient cells. Growing evidence indicates that EVs originating from cardiovascular cells as well as distant organs, including the liver, kidney, adipose tissue, lung, and intestine, participate in cardiac aging by influencing senescence-associated signaling, chronic inflammation, mitochondrial and metabolic dysfunction, fibrosis, microvascular remodeling, and contractile function. In this review, we outline the biological basis of circulating EVs in cardiac aging, describe their cellular and inter-organ sources, and examine how they promote progressive myocardial remodeling. We also consider their potential as biomarkers for cardiac aging and age-related heart disease, along with emerging therapeutic strategies such as blocking pathogenic EV signals, using reparative or engineered EVs, and implementing systemic interventions that modulate EV-mediated communication. Key translational challenges are highlighted, including EV heterogeneity, low tissue specificity, methodological inconsistencies, and the need to distinguish physiological cardiac aging from accelerated aging and age-related cardiovascular disease, as EV profiles may reflect systemic comorbidities rather than intrinsic cardiac aging. A deeper understanding of systemic EV crosstalk may offer new insights into the aging heart and support more precise methods for risk stratification, monitoring, and intervention.

Cardiac fibrosis is one of the main causes of mortality from cardiovascular disorders and may result in heart failure, irregular heartbeats, and sudden cardiac death. Multiple complex mechanisms involved in cardiac fibrosis are beyond the scope of current treatments. Inflammasomes are significant inflammatory modulators. Inflammasome impairment may exacerbate heart failure. The most specific inflammasome associated with inflammatory and cardiovascular disorders is Nucleotide-binding oligomerisation domain leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3). Pathogen-associated molecular patterns and damage-associated patterns are recognised by the intracellular sensor NLRP3, which causes the NLRP3 inflammasome to assemble and become active. Thus, a greater awareness of the pathological function of the inflammasome in heart fibrosis may lead to new approaches to the disease's early detection and management. Understanding the inflammasome's regulatory functions in fibrosis of the heart in its entire form has been made possible by recent research on the subject. The most recent studies on the roles of the NLRP3 inflammasome in different cardiac conditions are included in this review. According to recent research, the NLRP3 inflammasome promotes a number of inflammatory reactions and is linked to myofibroblast development, mitochondrial modulation, and pyroptosis in cardiac fibrosis. These discoveries provide light on the critical function of the NLRP3 inflammasome in the aetiology of heart fibrosis, which may help establish novel paths for therapy and prevention.

To compare the effects of various exercise modalities and doses on left ventricular ejection fraction (LVEF) in patients with heart failure. We systematically searched eight electronic databases through December 2025. Randomized controlled trials involving adult HF patients were eligible. Interventions comprised aerobic exercise (AE), resistance training (RT), combined exercise (CE), mind-body exercise (ME), high-intensity interval training (HIIT), and control. Random-effects network meta-analysis was employed to estimate mean differences with 95% credible intervals, and surface under the cumulative ranking curve probabilities were calculated. Nonlinear dose-response relationships were modeled using MET-minutes per week. 42 RCTs comprising 3,519 participants were included. Network meta-analysis demonstrated that all exercise modalities significantly improved LVEF compared with control. Resistance training showed the largest treatment effect (MD: 9.9; 95% CrI: 6.5, 13.0), followed by HIIT (MD: 8.4; 95% CrI: 4.2, 12.0), CE (MD: 6.0; 95% CrI: 2.9, 9.0), and AE (MD: 5.2; 95% CrI: 3.3, 7.1). SUCRA rankings indicated RT had the highest probability of being optimal (93.1%), followed by HIIT (76.1%), ME (55.3%), CE (46.0%), and AE (29.5%). Dose-response analysis revealed a non-linear quadratic relationship between MET-minutes per week and LVEF improvement. The minimum effective dose was 280 MET-minutes/week, with the optimal dosage range of 500-800 MET-minutes/week. Modality-specific patterns emerged: RT produced benefits at low doses (220 MET-minutes/week; optimal 330-440), whereas HIIT required higher thresholds (440 MET-minutes/week; optimal 560-780). Evidence certainty ranged from very low to moderate across comparisons per CINeMA framework. Resistance training is the most effective exercise modality for improving LVEF in HF patients, particularly at low-to-moderate doses. These findings support a precision-based rehabilitation strategy centered on RT to optimize cardiac function. PROSPERO, CRD420261329239.

Cardiac surgery remains a high-risk intervention, with postoperative complications, including ischemic events (myocardial infarction and stroke), acute kidney injury, respiratory failure, and neurocognitive dysfunction, affecting up to 30% of patients and resulting in increased mortality. While inhaled nitric oxide (NO) is traditionally used for pulmonary hypertension and right ventricular dysfunction, recent experimental and clinical studies suggest its organ-protective potential may mitigate ischemia-reperfusion injury and hemolysis induced toxicity. However, whether these physiological and mechanistic effects translate into improved patient-centered outcomes remains unproven in a large-scale setting. The NORISC trial aims to determine whether perioperative NO administration reduces major complications requiring intensive life support following cardiac surgery. This is an international, multicenter, double-blind, randomized (1:1), parallel-arm superiority trial. We will enroll 3650 patients undergoing elective cardiac surgery with cardiopulmonary bypass (CPB). The intervention group will receive NO at 80 parts per million (ppm) via the oxygenator sweep gas during CPB, followed by inhaled NO at 40-80 ppm via mechanical ventilation for up to 6 hours postoperatively or until extubation, whichever occurs first. The control group will receive standard care with placebo gas. The primary outcome is a 30-d composite of all-cause mortality and major adverse events (MAEs) necessitating intensive life support (e.g., stage 3 AKI, mechanical circulatory support, or prolonged ventilation, etc). Based on a hypothesized 20% relative risk reduction (from 20% to 16%), a sample size of 3650 provides 80% power at a one-sided α of 0.025. Conclusion/Expected Impact: The NORISC trial will provide high-quality, definitive evidence on the clinical efficacy of NO in cardiac surgery. By targeting hemolysis-mediated organ injury through a standardized delivery strategy, this study has the potential to redefine perioperative management and reduce the global burden of postoperative morbidity. The protocol has received Institutional Review Board approval at all participating centers. Recruitment commenced in May 2025. Results will be disseminated through peer-reviewed publications and international scientific congresses. ClinicalTrials.gov NCT06702553.

Coronary artery disease (CAD) and ischemic mitral regurgitation (IMR) commonly co-exist, yet the optimal intervention for these patients is unclear. Herein, we perform a systematic review and meta-analysis comparing the outcomes of patients with multivessel CAD and IMR undergoing coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI). PubMed and Embase were systematically searched for articles comparing outcomes of patients with CAD and IMR undergoing revascularization with CABG or PCI, with or without concomitant mitral valve interventions. Thousand two hundred eighty-five studies were identified and 8 were included in this review after full text review. The primary outcome of this study was mortality, and secondary outcomes included myocardial infarction, stroke, heart failure hospitalizations, and residual or recurrent mitral regurgitation. Pooled analyses identified no significant differences in long-term mortality [odds ratio (OR): 1.13, 95% confidence interval (CI): 0.77-1.68, P = 0.53] with considerable heterogeneity between studies. However, following the exclusion of a single outlier, heterogeneity in the pooled analysis of long-term mortality improved and the outcome favored CABG over PCI (OR: 1.39, 95% CI: 1.06-1.83, P = 0.02). Rehospitalization for heart failure also favored CABG (OR: 1.49, 95% CI: 1.16-1.92, P = 0.002). This systematic review and meta-analysis suggested lower rates of long-term mortality and heart failure hospitalizations for CABG compared to PCI. CABG remains preferrable for patients with acceptable surgical risk, multivessel CAD, and IMR.

Chemotherapy-induced cardiotoxicity is a major contributor to long-term cardiovascular morbidity among cancer survivors. ACE inhibitors (ACEIs), angiotensin receptor blockers and beta blockers have been proposed as prophylactic therapies; however, the robustness of existing evidence is unclear. We aimed to evaluate the strength, consistency and certainty of evidence from meta-analyses of randomised controlled trials (RCTs) assessing antihypertensive agents for preventing chemotherapy-related cardiac dysfunction. We conducted an umbrella review of meta-analyses of RCTs following Preferred Reporting Items for Overviews of Reviews guidelines. Systematic searches were performed in PubMed, Embase and Cochrane Database through May 2025. Data were extracted and reanalysed using random-effects models (DerSimonian-Laird if &#x2265;10 studies; Hartung-Knapp-Sidik-Jonkman if <10). Certainty of evidence was graded using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework. Primary outcomes included measures of cardiac function and structure; secondary outcomes were clinical and adverse events. 35 meta-analyses comprising 108 associations were included. Preservation of left ventricular (LV) ejection fraction was observed with ACEIs (mean difference, MD, 4.22%, 95%&#x2009;CI 1.56% to 6.88%; GRADE: very low) and beta blockers (MD 2.77%, 95%&#x2009;CI 1.40% to 4.14%; low). Beta blockers reduced ratio of the early (E-wave) to late (A-wave) velocity decline (MD 0.07, 95%&#x2009;CI 0.01 to 0.13; moderate). No significant effect was noted on LV dimensions or biomarkers. Beta blockers reduced incidence of heart failure (relative risk, RR, 0.29, 95%&#x2009;CI 0.26 to 0.34)&#x2009;and cardiotoxicity (RR 0.44, 95%&#x2009;CI 0.26 to 0.75), while ACEIs reduced arrhythmias (RR 0.17, 95%&#x2009;CI 0.03 to 0.91); certainty was low. No significant impact was detected on all-cause mortality or hypotension. ACEIs and beta blockers appear to confer modest cardioprotective effects during chemotherapy, particularly regarding systolic function and heart failure incidence, although with predominantly low-certainty evidence. Larger, robust RCTs with standardised endpoints are required before routine prophylactic use is recommended. CRD420251046471.

Myocarditis and pericarditis represent a broad spectrum of inflammatory heart diseases and are important differential diagnoses in patients presenting with chest pain, heart failure, or arrhythmias. Diagnosis is often challenging due to non-specific clinical presentation and biomarkers. Growing recognition of the clinical relevance of myocardial inflammation, together with accumulating evidence, has led to increased scientific and clinical attention. This is reflected in emerging concepts such as the introduction of the new term "inflammatory myocardial syndrome (IMPS)" in the recently published guidelines of the European Society of Cardiology (ESC). Notably, these are the first ESC guidelines to cover the full spectrum of inflammatory diseases of the myocardium and pericardium - marking an important paradigm shift in the field. Current ESC guidelines highlight the central role of multimodality cardiac imaging in the evaluation of myocardial inflammation. While echocardiography serves as a first-line tool, cardiac magnetic resonance imaging (CMR) is considered the non-invasive gold standard for tissue characterization. Nuclear imaging techniques such as positron emission tomography (PET) are increasingly relevant, particularly in specific entities such as cardiac sarcoidosis. This review highlights the practical role of multimodality imaging in the diagnostic work-up of myocardial inflammation, with emphasis on clinically relevant decision-making. Inflammatorische Herzerkrankung. Myokarditis und Perikarditis umfassen ein breites Spektrum entz&#xfc;ndlicher Herzerkrankungen und sind wichtige Differentialdiagnosen bei Thoraxschmerzen, Herzinsuffizienz und Rhythmusst&#xf6;rungen. Die Diagnosestellung ist h&#xe4;ufig herausfordernd, da klinische Pr&#xe4;sentation und Biomarker unspezifisch sein k&#xf6;nnen. Neue wissenschaftliche Erkenntnisse und die zunehmende klinische Relevanz myokardialer Inflammation haben zu einer Weiterentwicklung diagnostischer Konzepte gef&#xfc;hrt, einschliesslich der Einf&#xfc;hrung des Begriffs &#xab;inflammatorisches myoperikardiales Syndrom (IMPS)&#xbb;. Erstmals decken die aktuellen Leitlinien der Europ&#xe4;ischen Gesellschaft f&#xfc;r Kardiologie (ESC) das gesamte Spektrum entz&#xfc;ndlicher Erkrankungen von Myokard und Perikard gemeinsam ab &#x2013; ein wichtiger Paradigmenwechsel in der klinischen Praxis. Die ESC-Leitlinien betonen die zentrale Rolle der multimodalen kardialen Bildgebung in der diagnostischen Abkl&#xe4;rung. W&#xe4;hrend die Echokardiographie als prim&#xe4;re Screeningmethode dient, stellt die kardiale Magnetresonanztomographie (MRT) den nicht-invasiven Goldstandard zur Gewebecharakterisierung dar. Nuklearmedizinische Verfahren wie die Positronen-Emissions-Tomographie (PET) gewinnen insbesondere bei spezifischen Formen wie der kardialen Sarkoidose zunehmend an Bedeutung. Dieser &#xdc;bersichtsartikel beleuchtet die aktuellen Entwicklungen und legt dabei einen besonderen Fokus auf die klinische Anwendung bildgebender Verfahren in der diagnostischen Abkl&#xe4;rung. Schl&#xfc;sselw&#xf6;rter: Myokarditis, Perikarditis, kardiale Bildgebung, kardiale Magnetresonanztomographie (MRT), Positronen-Emissions-Tomographie (PET), Inflammatorisches myoperikardiales Syndrom (IMPS).

Influenza infection is a significant cause of global illness and death. Although mainly a respiratory disease, it can be complicated by extra-pulmonary conditions like myocarditis and myopericarditis. The prevalence and range of influenza-associated myocarditis are not well understood, especially in the Middle East, where case reports are limited. We conducted a retrospective case series of adult patients admitted to King Abdulaziz Medical City in Riyadh, Saudi Arabia, from September 2024 to July 2025, with clinically diagnosed influenza-associated myocarditis. Diagnosis was based on the 2024 ACC Expert Consensus Decision Pathway criteria and a positive influenza PCR. Clinical data, diagnostic results, management strategies, and outcomes were collected from electronic medical records. Additionally, we performed a structured literature review of case reports and case series on influenza-associated myocarditis to provide context for our findings. Four patients (ages 37-79 years; three women) were identified with clinically diagnosed influenza-associated myocarditis. Presentations ranged from mild myopericarditis with preserved hemodynamics to fulminant myocarditis complicated by cardiogenic shock requiring venoarterial extracorporeal membrane oxygenation and Impella support. All patients received oseltamivir, and selected patients received colchicine, nonsteroidal anti-inflammatory drugs, or immunomodulatory therapy. Three patients recovered with normalization of cardiac function, while one patient with fulminant disease died despite aggressive support. The literature review identified 24 published cases of influenza-associated myocarditis. Most patients were previously healthy young adults (median age 42.5 years), and 79.2% achieved complete recovery. However, 20.8% died, often following rapid progression to cardiogenic shock and multi-organ failure. Influenza-associated myocarditis is a rare, potentially fatal complication affecting healthy adults. Our findings highlight the importance of early recognition, prompt antiviral therapy, and access to mechanical circulatory support when needed. This case series, among the first from Saudi Arabia, along with a literature review, offers insights into the clinical spectrum, management, and outcomes of this underrecognized condition.

Acute myocardial infarction (AMI), which causes cardiomyocyte death due to ischemia, affects &#x223c;7 million people annually worldwide, and its mortality rate is greater than one-third. Furthermore, AMI severely impairs cardiac function, leading to heart failure and fatal arrhythmias. While timely reperfusion improves survival, adverse remodeling and subsequent heart failure remain major challenges. After cardiomyocyte death, excessive fibrosis in and around the infarct decreases heart size and impairs cardiac function, leading to heart failure. Current end-stage treatments (e.g., drugs and devices) cannot repair damaged tissue, but injectable biomaterials, particularly hydrogels, offer promising new therapeutic strategies; their excellent biocompatibility, degradability, high water content, and injectability allow the targeted delivery of bioactive molecules, drugs, cells, and exosomes (exos) directly into the damaged myocardium to promote repair after AMI. Here, we describe the mechanism of progression from coronary atherosclerotic heart disease to myocardial infarction and myocardial injury and the superiority of hydrogels for treating this disease. We also discuss the mechanisms of action of different bioactive molecules, drugs, cells, exos, miRNA and two therapeutic agents-loaded hydrogels for treating myocardial injury and the experimental effects of these hydrogels. Finally, we discuss the existing problems associated with injectable hydrogels and the prospects of using hydrogel formulations in the treatment of myocardial infarction.

Heart failure (HF) continues to be a major global health burden, with persistent morbidity and mortality despite guideline-directed and device-based therapies. Evidence suggests the gut-heart axis is a critical and underrecognized contributor to HF progression. Alterations in cardiac output and systemic venous congestion in HF lead to intestinal hypoperfusion, mucosal edema, and loss of barrier integrity, increasing intestinal permeability, gut dysbiosis, and translocation of microbial products. This systemic translocation is associated with chronic low-grade inflammation that activates innate immune pathways that correlate with endothelial dysfunction, oxidative stress, fibroblast activation, and adverse cardiac remodeling. Gut-derived metabolites derived by microbial metabolism modulate cardiovascular health by altering the metabolic profiles. Dysbiosis results in loss of protective short-chain fatty acid (SCFA)-producing bacteria and enriches pro-inflammatory taxa such as trimethylamine N-oxide (TMAO)-producing bacteria. Elevated TMAO is associated with increased mortality and hospitalization in HF, whereas SCFAs enhance barrier integrity and immune tolerance. Secondary bile acids and uremic toxins such as indoxyl sulfate and p-cresyl sulfate further link dysbiosis to fibrosis and vascular stiffness. Circulating markers such as TMAO, lipopolysaccharide-binding protein (LBP), and soluble CD14 carry prognostic value beyond traditional cardiac biomarkers. This review highlights current experimental, translational, and clinical evidence describing gut dysbiosis and its molecular links to HF progression. Targeting the gut-heart axis represents a novel therapeutic approach in HF. Dietary modulation, probiotics/prebiotics, fecal microbiota transplantation, and inhibitors of microbial metabolic pathways show promise. Future research should emphasize microbiota-based interventions in HF management.