Search Results (192)

Background: Influenza is primarily a respiratory illness, but it is increasingly linked to acute cardiovascular complications, including myocarditis and sudden cardiac death. Evidence on influenza-associated cardiac involvement remains fragmented and largely derived from case-based reports. Methods: This systematic review followed PRISMA guidelines and was registered with PROSPERO (CRD420251249130). PubMed, Web of Science, and Google Scholar were searched for eligible studies. Case reports and case series were included to characterize rare, severe, or atypical cardiac manifestations that are not captured in larger epidemiological studies. Data on demographics, influenza subtype, cardiac manifestations, investigations, management, and outcomes were extracted. Results: Thirty-three studies (32 case reports and one case series) comprising 36 cases were included. Influenza A was reported in 26 cases and influenza B was reported in 9 cases. Myocarditis was the most common manifestation (19 cases, 53%), including fulminant myocarditis in 9 cases (25%). Cardiogenic shock occurred in seven cases (19%), malignant arrhythmias in four(11%), myocardial infarction–like presentations in three (8%), and cardiac arrest or sudden cardiac death in six cases (17%). Cardiac involvement occurred across all age groups, frequently in patients without pre-existing coronary artery disease. Overall mortality was 44% (16/36), with fatalities reported in both influenza A and B infections. These findings predominantly reflect severe and published cases and may not represent the full clinical spectrum of influenza-associated cardiac involvement. Conclusions: This review highlights that influenza infection has been reported in association with a range of acute cardiac manifestations, particularly myocarditis, including severe and fulminant presentations. However, given the reliance on case reports and case series, the findings are subject to significant publication bias and do not permit the estimation of incidence, risk, or causal inference. These observations should therefore be interpreted as hypothesis-generating. Full article

Background/Objectives: Children with congenital long QT syndrome (cLQTS) are at extremely high risk of torsades de pointes (TdP) and sudden cardiac death (SCD). Although the implantable cardioverter-defibrillator (ICD) is a cornerstone in SCD prevention, traditional transvenous ICDs are associated with venous access occupation, lead wear or fracture due to somatic growth, and difficulties with long-term lead revision or extraction. The extravascular ICD, which places the lead in the substernal extravascular space, has the potential to circumvent these lead-related complications. We report the experience of successful extravascular ICD implantation in a young child with drug-refractory cLQTS type 2 (cLQTS2). Methods: The clinical data of a 9-year-old boy with cLQTS2 were retrospectively analyzed. The patient carried a heterozygous KCNH2 variant (c.1810G>A, p.Gly604Ser) and had been on long-term oral propranolol and mexiletine. He presented with a cardiac arrest out of hospital during nocturnal sleep, was transferred to our hospital after successful cardiopulmonary resuscitation, and had TdP captured on ambulatory monitoring. Following multidisciplinary discussion, preoperative chest computed tomography (CT) assessment of the substernal anatomy, and informed consent, extravascular ICD implantation was performed on hospital day 11. The procedure involved the creation of a substernal tunnel via a subxiphoid incision, placement of the defibrillation lead in the anterior mediastinum with lead slack reserved for growth, and positioning of the pulse generator in a left axillary subcutaneous pocket. Intraoperative defibrillation testing succeeded with a single 30 J shock. Results: The postoperative recovery was uneventful without procedure-related complications. At the 2-month follow-up, device parameters were satisfactory and no inappropriate shocks had occurred. The corrected QT interval (QTc) decreased from 563 ms on admission to 522 ms. Ambulatory monitoring detected asymptomatic episodes of non-sustained ventricular tachycardia, but no ventricular fibrillation or syncope was observed. Venous access was fully preserved. Conclusions: In children with drug-refractory cLQTS2, the extravascular ICD provides defibrillation and antitachycardia pacing (ATP) while avoiding transvenous lead complications and preserving venous access. This case shows that with precise preoperative planning and lead redundancy, the device appears feasible and can be implanted without short-term complications in young children. Larger studies with longer follow-up are needed to evaluate long-term device performance. Full article

Background: Anomalous origin of the right coronary artery from the pulmonary artery (ARCAPA) is an extremely rare and potentially fatal congenital heart defect, accounting for approximately 0.003% of all coronary artery anomalies. Methods: A literature search was performed in the PubMed and eLibrary databases using the keywords “ARCAPA” and “anomalous origin of the right coronary artery from the pulmonary artery” for the period from 2005 to 2025. A total of 158 papers were screened, from which 57 articles reporting 59 clinical cases in adult patients were selected. Results: The median age was 55 years [18–80]. Males accounted for 54.2% (32/59). ARCAPA was an incidental finding during evaluation for another condition in 35.9% (21/59) of cases. Clinical presentation: retrosternal pain—47.5% (28/59), dyspnea—44.1% (26/59), and reduced exercise tolerance—35.9% (21/59). A completely asymptomatic course was observed in 22.0% (13/59) of patients. In rare cases, the initial presenting manifestations included atrial fibrillation, cardiac arrest during a marathon, and worsening dyspnea during pregnancy. The most commonly used diagnostic modalities were computed tomography angiography—in 67.8% (40/59) of cases—and coronary angiography—in 49.2% (29/59) of cases. Cardiac catheterization confirmed the diagnosis in only 10.2% (6/59) of patients. Surgical correction was performed in 54.2% (32/59) of patients; the most frequently used technique was reimplantation of the right coronary artery into the ascending aorta—in 42.4% (25/59) of cases. One long-term complication was recorded—right coronary artery thrombosis 17 years after surgery—and one case of sudden cardiac death occurred in an unoperated patient. Conservative management was chosen in 40.7% (24/59) of patients, mainly due to an asymptomatic course, high surgical risk, or patient refusal. Conclusions: ARCAPA is a rare anomaly for which surgical treatment appears to be the preferred approach in symptomatic patients or those with documented ischemia, while conservative management may be acceptable in selected asymptomatic patients. Conservative management is acceptable in truly asymptomatic patients, but regular follow-up is recommended. Full article

Background: Inherited arrhythmic syndromes (IAS) are an important but under-recognized cause of sudden cardiac death (SCD), particularly in younger individuals. Understanding long-term mortality trends is essential to evaluate their public health impact. Objective: To assess temporal trends and demographic disparities of IAS-related sudden cardiac death among individuals aged 5–44 years in the United States using CDC WONDER data. Methods: This retrospective observational study utilized the CDC WONDER Multiple Cause-of-Death database from 1999 to 2024. Deaths were identified using ICD-10 codes for non-ischemic arrhythmogenic conditions (I42, I44, I45, I47, I49) in combination with sudden cardiac arrest or unexplained death (I46, R96). Ischemic heart disease (I20–I25) was excluded to enhance specificity for inherited causes. Crude and age-adjusted mortality rates (AAMRs) per 1,000,000 population were calculated and stratified by age, sex, race/ethnicity, region, urbanization, and place of death. Joinpoint software helped us calculate the average annual percentage change (AAPC)/annual percent change (APC) in AAMRs and the 95% CIs for these changes. Results: A total of 8879 deaths were identified over the study period. The AAMR increased from 1.46 (95% CI: 1.27–1.64) in 1999 to 3.15 (95% CI: 2.89–3.42) in 2024, peaking at 4.54 in 2021, with an overall AAPC of 3.71% (p < 0.000001). Mortality was higher in males; however, females demonstrated a greater relative increase over time. Non-Hispanic Black individuals exhibited the highest mortality rates and fastest rise. The 25–44-year age group accounted for most deaths and showed the steepest increase. Regional and urban–rural disparities were observed, with higher mortality rates in the South and rural areas. Conclusions: It is concluded that mortality related to inherited arrhythmic syndromes and sudden cardiac death is rising among young individuals in the United States. The findings highlight a growing burden of potentially inherited arrhythmogenic conditions and underscore the need for early detection strategies, including genetic screening and targeted public health interventions, to reduce premature cardiovascular mortality. Full article

Background: Firefighting is a hazardous occupation, yet data online-of-duty deaths in European firefighter populations remain limited. This study aimed to characterise the mechanisms and circumstances of firefighter fatalities in Poland and to estimate exposure-based fatality rates, with particular attention to differences between career and volunteer personnel. Methods: In this retrospective observational study, line-of-duty firefighter fatalities in Poland from 1995 to 2025 were identified from a nationwide repository and cross-validated against official sources. The mechanism of death was classified from case narratives following the Utstein framework. Group comparisons used chi-square, Fisher’s exact, and Welch’s tests; multivariable probit regression assessed predictors of mechanism; and per-capita and per-deployment fatality rates were computed using national denominator data. Results: Of 112 fatalities, 73 (65.2%) involved volunteer firefighters. Sudden Cardiac Arrest of Presumed Non-Traumatic origin (SCA-PNT) was the leading mechanism (44.6%), followed by traumatic injury (37.5%). Volunteers were older than career firefighters (46.4 ± 14.0 vs. 34.6 ± 8.7 years; p < 0.001) and more likely to die of SCA-PNT (odds ratio 6.35; 95% confidence interval 2.46–16.40) and during the response phase (odds ratio 5.07; 1.89–13.55). Age was the strongest independent predictor of mechanism. The per-capita fatality rate was higher among career firefighters (incidence rate ratio 5.16), whereas the per-deployment rate was higher among volunteers (incidence rate ratio 2.25). Conclusions: Firefighter mortality in Poland differs by employment status and is strongly age-dependent. Age-stratified cardiovascular surveillance and prevention may be more effective than formation-based approaches. Full article

Perioperative anaphylaxis, though rare, is a potentially life-threatening complication. While antibiotics and neuromuscular blocking agents are common triggers, benzodiazepine-induced reactions have been considered uncommon. Remimazolam, a novel benzodiazepine sedative, has gained widespread use in Korea due to its rapid onset, short recovery, hemodynamic stability, and availability of flumazenil. However, increasing utilization has coincided with rising reports of hypersensitivity. We report the case of a 62-year-old female undergoing contralateral total knee replacement under spinal anesthesia. Continuous remimazolam infusion was initiated, but within ten minutes the patient developed chest discomfort followed by abrupt hypotension and oxygen desaturation, requiring urgent conversion to general anesthesia. Following a remimazolam bolus and rocuronium administration, sudden cardiac arrest occurred. Return of spontaneous circulation (ROSC) was achieved after approximately 28 min of cardiopulmonary resuscitation with a cumulative intravenous epinephrine dose of approximately 17 mg, and veno-arterial extracorporeal membrane oxygenation (ECMO) was required. Post-ROSC transesophageal echocardiography demonstrated a transient anteroseptal regional wall motion abnormality; subsequent coronary angiography demonstrated no significant coronary disease, and computed tomography pulmonary angiography was negative for embolism, leaving acute hypersensitivity as the most plausible mechanism. Acute serum tryptase was elevated at 11.6 µg/L and normalized to 3.4 µg/L (the patient’s individual baseline) prior to discharge, satisfying the World Allergy Organization (WAO) criterion. A skin prick test performed four weeks later was positive for remimazolam and negative for rocuronium and the other coadministered agents. An expanded multi-database literature review identified 16 prior cases of remimazolam-induced anaphylaxis. Most described cardiovascular collapse as the predominant manifestation. To our knowledge, based on available literature, this is among the first reports of remimazolam-induced anaphylaxis occurring in the setting of high spinal anesthesia with sympathetic blockade. Vigilance and adherence to established anaphylaxis management guidelines are essential. Full article

Background: Although less frequently encountered, aortic valve stenosis is associated with complications separate from its hemodynamic burdens, such as infective endocarditis. Case Summary: We report the case of a 77-year-old female patient with regular cardiac follow-up in the setting of an asymptomatic severe aortic stenosis, who presented to the emergency department with signs and symptoms of sepsis and acute decompensated heart failure. Echocardiography revealed two vegetations attached to the tricuspid valve, an abscess of the anterior aortic ring, and a high-velocity ventricular septal defect. The patient was started on adequate antibiotic therapy. Surgical treatment in an urgent manner (within a few days) was decided by the Heart Team, in accordance with the ESC guidelines on the management of infective endocarditis. Whilst awaiting surgery, the patient presented with a sudden hemodynamic deterioration a few days after diagnosis, with cardiopulmonary arrest and subsequent death. Discussion: We hypothesize that the patient developed an infective endocarditis of the degenerated stenotic aortic valve with extension from left to right via a ventricular septal defect, the development of which was facilitated by the high trans-aortic valve gradient. Some reported cases describe a ventricular septal defect as a complication of native aortic valve endocarditis, though not all involve concomitant aortic stenosis. In conclusion, our case illustrates a very rare scenario of infective endocarditis complicating aortic stenosis with fulminant development. This case highlights a rare, albeit severe complication associated with aortic stenosis and therapeutic challenges in managing the dismal evolution of endocarditis in this setting. Full article

Background: Thrombotic disorders remain one of the leading causes of global mortality, necessitating the discovery of anticoagulants with broader therapeutic windows and multi-target efficacy. This study aimed to identify FDA-approved drugs capable of simultaneously inhibiting three critical nodes of the coagulation cascade: Factor X (F10), Proteinase-activated receptor 1 (PAR1) and Prothrombin (F2). Methods: High-confidence 3D structures of coagulation cascade proteins were established using AlphaFold2 and validated via MolProbity (Favored regions > 91%). A library of 1657 compounds from the Zinc database was screened using PyRx, followed by rigorous ADMET profiling to evaluate pharmacokinetic viability. The structural integrity and binding kinetics of the top candidate drugs were further analyzed through Molecular Dynamics simulation for 100 ns. Results: Virtual screening and downstream analysis identified 30 multi-target drugs. Avodart and Naldemedine were observed to have superior pharmacokinetic equilibrium. Compared to the other two drugs (Digoxin and Ledipasvir), Avodart and Naldemedine showed high affinity, higher adherence to drug likeness, lower metabolic inhibition risks and lack of acute toxicity, and were therefore the most suitable candidates. The 100 ns MD simulations revealed Avodart and Naldemedine to have the highest level of interaction stability and favorable MM-GBSA energies with Factor X, whereas Ledipasvir and Digoxin exhibited significant structural instability. Conclusions: The study proposes Avodart and Naldemedine as promising candidates for drug repurposing in antithrombotic therapy. This study provides a computational blueprint for the development of next-generation, broad-spectrum anticoagulants. Full article

Background: Brugada Syndrome (BrS) is a cardiac arrhythmia associated with an increased risk of ventricular arrhythmias and sudden cardiac arrest. Although the arrhythmic substrate is traditionally localized to the ventricles, atrial fibrillation (AF) is frequently observed, suggesting a shared molecular substrate between atrial and ventricular arrhythmias. C-type natriuretic peptide (CNP) and related microRNAs (miRNAs) modulate atrial and ventricular physiology, but their roles in exosomes in BrS have not been investigated. Objectives: To investigate alterations in CNP mRNA expression and changes in the expression of selected CNP-associated miRNAs implicated in AF, both analyzed in exosomes isolated from individuals with BrS and from healthy controls. Methods: Exosomes were isolated from the plasma of BrS patients without a history of overt AF and from healthy controls. In silico analyses identified CNP-targeting miRNAs implicated in AF. Exosomal CNP and CNP-related miRNAs were analyzed using Droplet Digital PCR. Results: BrS patients exhibited a significant increase in exosomal CNP mRNA expression levels compared with controls. MiR-138-5p was selectively downregulated, whereas other AF-related CNP-targeting miRNAs (miR-4443, miR-206, miR-142-5p, miR-223-5p) showed comparable levels between groups. A positive correlation between exosomal CNP and miR-223-5p and miR-4443 suggests shared regulatory pathways. Conclusions: these findings indicate that exosomal profiling may provide a more sensitive approach than conventional circulating measurements to detect molecular remodeling in BrS. The observed alterations highlight a potential shared molecular substrate between atrial and ventricular arrhythmias and may inform future studies aimed at refining diagnostics and developing targeted therapeutic strategies. Full article

Brugada syndrome (BrS) is a rare but potentially life-threatening condition that may lead to sudden cardiac death. Among the causes, dysfunctions of ion channels involved in the cardiac action potential (specifically in SCN5A and SCN10A genes) are particularly significant. Among diagnosed Brugada patients, fever-induced episodes occur in 20–30% of cases. Fever worsens sodium channel dysfunction, as elevated temperature further reduces their conductance. First clinical manifestation of BrS occurs usually during a febrile episode, especially in young people. We performed a multiparametric examination in addition to genetic analysis. We treated a 19-year-old man presenting with subfebrility. During the patient’s subfebrile episodes, 12-lead ECG recordings revealed ST-segment elevations in leads V1–V3. Notably, the patient remained asymptomatic. Targeted genetic testing of SCN5A did not reveal any disease-causing variants as an underlying cause of the syndrome, but the temperature-inducing effect was demonstrated. The occurrence of the Brugada type 1 pattern has also been observed at subfebrile episodes, although significantly rarely. This case demonstrates that in susceptible patients, even a relatively mild elevation in body temperature can trigger ion channel dysfunctions. Timely diagnosis and follow-up are important in preserving quality of life and preventing fatal outcomes. Full article

Pulmonary hypertension (PH) can be defined as a mean pulmonary artery pressure (mPAP) greater than 20 mm Hg at rest during right heart catheterization (RHC). The reported prevalence of PH throughout the globe has been estimated to impact approximately 1% of the total population, with a majority of those afflicted being women more than men. Numerous etiologies give rise to the pathophysiology of PH, including heart disease (i.e., left-sided heart failure), lung diseases, and other unclear causes related to chronic stages and complications surrounding long-standing pulmonary thromboembolisms, side effects of certain medications, and genetic and environmental factors. Untreated PH can lead to severe morbidities such as cardio-renal syndrome and congestive hepatopathy (cardiac cirrhosis). Management of PH focuses on decreasing pulmonary pressures by using vasodilators such as prostanoids, and phosphodiesterase type 5 (PDE-5) inhibitors, as well as newer treatments such as sotatercept, which inhibits activin signaling, thereby inhibiting excessive cell growth in the pulmonary artery vasculature and down-regulating the pro-proliferative pathways. Full article

Cardiac arrest is a way of demise of patients who are affected by heart failure (HF), being more frequent in those with HF with a reduced left ventricular ejection fraction (HFrEF), and is, as such, responsible for 30–50% of cardiac death. Specific data on the risk of sudden cardiac death (SCD) related to HF with a preserved ejection fraction (HFpEF) and HF with a mildly reduced ejection fraction (HFmrEF) are lacking, as well as data regarding ventricular arrhythmias in this population. Considering the 0.3% person/year incidence rate of investigator-reported ventricular tachycardia (VT) and ventricular fibrillation (VF), the rate of SCD in the analyzed population seems to be 1.3% per year. Age, gender, history of diabetes and myocardial infarction, left bundle branch block (LBBB) on electrocardiogram (ECG), and a natural logarithm of N-terminal pro B-type natriuretic peptide (NT-proBNP), identified a subgroup of HFpEF patients with a higher risk (5-year cumulative incidence of 11%) of sudden death (SD). In HFpEF patients, both glifozins and finerenone did not demonstrate a beneficial effect on SCD incidence in comparison to placebo. A significantly lower rate of SCD emerged in patients who were treated with dapaglifozin (10 vs. 26 pts) among patients with HF with an improved ejection fraction (HFimpEF), who were defined as patients with a previous left ventricular ejection fraction (LVEF) < 40%. Promising methods discussed include cardiac magnetic resonance, myocardial scintigraphy, genetic assessment, and electrophysiologic studies for predicting SCD in those patients. In conclusion, arrhythmic SCD in HFpEF patients should not be considered merely as an effect of VT/VF; bradyarrhythmia is probably more frequent and dangerous. The effects of drugs in preventing SCD in HFpEF have not been demonstrated yet. Full article

Peripartum cardiomyopathy (PPCM) is a distinct condition that presents as heart failure (HF) in a woman who was previously healthy and has no prior cardiovascular issues. It results from idiopathic left ventricular (LV) dysfunction, characterized by a reduced LV ejection fraction below 45%. PPCM is a life-threatening condition with a high mortality rate (MR) that demands urgent treatment. Methods: This narrative review aims to define PPCM and its pathophysiology and conduct a scoping review of the latest data on the management of patients with peripartum cardiomyopathy during pregnancy and the postpartum period. Results: Currently, treatment follows standard HF protocols for reduced ejection fraction, with the possible addition of bromocriptine, and during pregnancy, medications that do not harm the fetus. Conclusions: Early, aggressive therapy is essential for a better prognosis, but managing PPCM can be challenging. Treatment of PPCM patients should be led by a team of highly qualified specialists, known as the Obstetric and Cardiac Care Team, comprising an obstetrician-perinatologist, an anesthesiologist, a cardiologist, and a cardiac intensive care specialist. Baseline left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) are the main prognostic factors. LVEF less than 30%, significant LV dilatation, LVEDD ≥ 6.0 cm, and right ventricular involvement are factors indicative of a poor prognosis. While pregnancy after PPCM is possible, it should be discouraged due to the significant risk of complications and even death. The most common causes of death in patients with PPCM are thromboembolic complications, severe HF, serious ventricular arrhythmias, cardiogenic shock, and sudden cardiac arrest. Full article

Background: Hypertrophic cardiomyopathy (HCM) is a common inherited disease and a leading known cause of sudden cardiac arrest in young adults and athletes. While genetic testing has advanced rapidly in the past decade, the yield of genetic testing remains low. The Clinical Genome Resource (ClinGen) initiative has become a leading resource for defining the clinical relevance of genetic variants with expert groups focusing on evaluating the strength of evidence for each HCM implicated gene. With the rise of large biobanks and population databases, genetic discovery has been significantly advanced. However, whether these databases can be used to validate gene–disease associations curated by ClinGen and provide evidence for novel gene–disease associations remains unclear. Objectives: Here, we utilized a publicly available database containing 748,879 individuals across three large biobanks (All of Us, UK biobank, Mass General Brigham biobank). Methods: We tested the association of rare coding variants in each gene in the HCM ClinGen panel with HCM. In total, 38 genes were tested, and Bonferroni correction was applied accordingly. Results: Of the 12 genes with definitive evidence for HCM (e.g., MYBPC3, MYH7, TNNT2, ALPK3), 8 (67%) demonstrated nominally significant association with HCM on a population level, and 5 (42%) remained significant after Bonferroni correction, further supporting the validity of these genes in HCM panels. Several definitive genes which are much less commonly affected in HCM (CSRP3, MYL3, ACTC1, TPM1, FHOD3, MYL2, and TNNC1) did not pass our Bonferroni corrected-significance threshold, but all had positively associated effect sizes with HCM. No genes deemed to have moderate or limited evidence had any significant associations with HCM even before Bonferroni correction. Conclusions: Altogether, we show that large biobanks and population databases generally recapitulate established gene–disease associations for HCM and support the ClinGen group’s gene curations. The utilization of such publicly accessible databases represents an additional tool for assessing gene validity in monogenic cardiac disorders with an established phenotype, although it may have limited sensitivity and should not be solely relied on. Full article

Out-of-hospital cardiac arrest (OHCA) remains a leading cause of sudden death worldwide, with wide variation in reported incidence and outcomes driven by heterogeneity in registries, emergency medical services (EMS) organization, and case definitions. Despite substantial advances in resuscitation systems, survival after EMS-treated OHCA generally remains below 10%, and outcomes are critically time dependent. Delays in emergency call activation, bystander cardiopulmonary resuscitation (CPR), and—most importantly—early defibrillation are associated with a rapid decline in return of spontaneous circulation and favorable neurological recovery. This narrative review synthesizes current evidence and implementation strategies aimed at reducing “time-to-CPR” and “time-to-shock,” with a specific focus on public-access defibrillation (PAD) as a tool to mitigate avoidable delay. Randomized trials and large registry studies consistently demonstrate that automated external defibrillator (AED) use before EMS arrival is a key determinant of survival in patients with shockable rhythms. However, the real-world effectiveness of PAD remains limited by suboptimal AED placement, restricted 24/7 accessibility, low public awareness, and underutilization driven by fear and lack of confidence. We compare different PAD delivery models—including EMS-based, police and first-responder-based, and fully integrated community systems—and summarize evidence supporting targeted, high-yield AED deployment and cost-effectiveness. In addition, we review emerging strategies to reduce avoidable delay and strengthen the early links of the chain of survival, such as school-based training programs, smartphone- and SMS-based citizen-responder networks, improved dispatch recognition of cardiac arrest (including artificial intelligence–supported tools), and drone-enabled AED delivery. Across these approaches, patient benefit critically depends on system integration, alert performance, and true AED accessibility. Finally, we describe the Italian “Progetto Vita” experience as a community-integrated model explicitly designed to minimize avoidable delay through widespread AED deployment, lay responder training, and real-time integration with EMS. We conclude by outlining future priorities, including the development of robust national OHCA registries and scalable solutions for the high burden of cardiac arrests occurring at home, such as population-level deployment of low-cost, ultra-portable AEDs. Full article