Search Results (36)

Background/Objectives: Syncope remains a common problem in the elderly, adversely affecting quality of life, morbidity and mortality. Diagnosis is challenging due to the atypical presentation, multifactorial aetiology, overlap with non-syncoptic falls and increased prevalence of cardiac disease. This study aims to investigate the impact of cardiac syncope in this high-risk population. Methods: A retrospective single-centre observational cohort study, including 171 patients ≥65 years old with syncope of unknown origin or other falls, was conducted. Different diagnostic tests and strategies were utilised during the investigational process, based on clinical judgement and the latest guidelines. Patients were classified either in the ‘high risk’ (‘cardiac’) or ‘low-risk’ (‘autonomic’) pathway. Results: Mean age was 76.4 ± 6.6 years (range: 65–92 years old) and the mean follow-up period was 40.5 months. Our study population was characterised by a high incidence of comorbidities and underlying heart disease, and polypharmacy. One third of the patients did not report prodromals, 81.9% had no recognisable trigger and 43.3% had various 12-lead ECG abnormalities. Overall, 67.8% of the patients were stratified in the ‘cardiac pathway’. Eventually, a final diagnosis was established in 126 patients (73.7%). The cause was cardiac syncope in 56.4%, reflex syncope in 26.2%, orthostatic hypotension in 7.9% and non-syncopal falls in 9.5%. An ILR was implanted in 90.1% with a diagnostic yield of 43%. ECG-based diagnosis occurred in 53.2% whereas time to diagnosis was 4.8 ± 3.3 months. Conclusions: Cardiac disease, mostly arrythmias, represent a common and possibly underestimated cause of unexplained syncope in the elderly. A structured approach including a targeted use of ILRs improves investigational process. Full article

Objective: To investigate long-term prognosis and impact factors in children with vasovagal syncope (VVS) receiving metoprolol therapy. Methods: This retrospective study included children with VVS who underwent metoprolol therapy at the Pediatric Syncope Unit of Peking University First Hospital between January 2012 and November 2023. Baseline demographic data, pre-treatment indices, including head-up tilt test (HUTT) and 24 h Holter monitoring, were collected. All participants received standardized metoprolol therapy for a minimum duration of one month. Follow-up was conducted between June and July 2025, with syncope recurrence as the primary endpoint. Multivariable Cox proportional hazards regression analysis was performed to identify independent impact factors of prognosis and to construct a Prognostic Risk Score (PRS) model. The model’s performance was rigorously validated through receiver operating characteristic (ROC) curve analysis, decision curve analysis (DCA), and Bootstrap resampling (1000 iterations). Furthermore, children were stratified into high- and low-risk groups based on median PRS values. Kaplan–Meier survival analysis was then performed to assess the model’s discriminative efficacy. Results: This study included 97 children diagnosed with VVS. The median duration of metoprolol therapy was 2.5 months (interquartile range [IQR]: 2.0–3.0 months), with a median follow-up period of 59 months (IQR: 25.5–72 months). During follow-up, syncope recurrence was observed in 37 patients, while 60 patients remained symptom-free. COX regression analysis showed that time-domain indices of heart rate variability (HRV), including the standard deviation of all NN intervals (SDNN) and the triangular index (TR), as well as the frequency-domain index of HRV very low frequency (VLF), were relative factors of the long-term prognosis in children with VVS treated with metoprolol. Based on the above three identified factors, the PRS model was calculated as: PRS = 0.03 × SDNN − 0.02 × VLF − 0.1 × TR. ROC showed that the area under the curve (AUC) for discriminative power related to long-term prognosis was 0.808 (p < 0.01). The cumulative recurrence rate of symptoms in the high-risk score group was significantly higher than that in the low-risk score group (p < 0.01). The DCA curve demonstrated the clinical applicability of the model. Bootstrap internal verification indicated high stability, with the bias-corrected and accelerated (Bca) confidence interval (CI) of the C index ranging from 0.71 to 0.89. Conclusions: After metoprolol treatment, 38.1% of children with VVS experienced syncope recurrence during a median follow-up period of 59 months. Baseline HRV index, SDNN, TR, and VLF were identified as factors associated with the long-term prognosis of children with VVS treated with metoprolol. The PRS model based on the above indices demonstrated good value in linking to the individual long-term prognosis. Full article

Background: Pulmonary embolism (PE) is a major cause of cardiovascular mortality, with heterogeneous presentation. Syncope, reported in 10–20% of cases, may indicate severe hemodynamic compromise, but its independent prognostic role remains uncertain. Methods: We retrospectively analyzed 300 patients admitted with acute PE confirmed by computed tomography pulmonary angiography between January 2022 and December 2024. Patients were stratified according to the presence of syncope at admission. Clinical, laboratory, and echocardiographic findings and outcomes were compared. Logistic regression was used to identify independent predictors of in-hospital mortality. The present study is a single-center, retrospective analysis. Results: Syncope occurred in 48 patients (16%). Compared with those without syncope, these patients had higher rates of right ventricular dysfunction (68.7% vs. 32.5%, p = 0.002), elevated troponin (75% vs. 44%, p = 0.01), hypotension (29% vs. 8%, p < 0.001), Intensive Care Unit (ICU) admission (56% vs. 22%, p < 0.001), and thrombolysis (19% vs. 8%, p = 0.03). In-hospital mortality was markedly higher in the syncope group (37.5% vs. 7.1%, p < 0.001). Multivariate analysis confirmed syncope as an independent predictor of mortality (OR 4.2, 95% CI 2.1–8.4, p < 0.001), alongside right ventricular dysfunction and elevated troponin. Conclusions: Syncope at presentation is a simple but powerful clinical marker of high-risk PE and should prompt intensive monitoring and consideration of early reperfusion therapy. Full article

This observational pilot study investigated neurocardiovascular responses to an active stand test using continuous physiological monitoring and functional data analysis (FDA) in older women. A sample of 25 community-dwelling female adults aged 59–78 years (mean age: 70.3 years) participated. Participants were dichotomized into comparison groups based on five factors: age (<70 vs. ≥70 years); the presence of initial orthostatic hypotension (IOH, yes/no); body mass index (BMI < 25 vs. ≥25 kg/m²); antihypertensive medication use (yes/no); and physical frailty status assessed by the Survey of Health, Ageing and Retirement in Europe—Frailty Instrument (SHARE-FI score < −0.5 vs. ≥−0.5). Each participant completed an active stand test during which six physiological signals were continuously recorded: systolic (sBP) and diastolic (dBP) blood pressure and heart rate (HR) via digital artery photoplethysmography and left frontal oxygenated hemoglobin (O₂Hb), deoxygenated hemoglobin (HHb), and tissue saturation index (TSI) via near-infrared spectroscopy (NIRS). The signal analysis focused on a standardized 200 s window spanning 50 s before to 150 s after the stand, with all signals resampled and synchronized at 5 Hz. FDA was used to statistically compare the full time series between groups for each signal. Group-level differences revealed that younger participants (<70 years) exhibited significantly higher HR in multiple periods following the stand (~10 s, ~30 s, ~90 s, and ~140 s post-stand) compared to their older counterparts. Participants with IOH demonstrated significantly lower sBP at ~10 s, ~80 s, and ~130 s post-stand and lower dBP at ~10 s post-stand. Among participants classified as overweight/obese (BMI ≥ 25 kg/m²), significantly lower levels of HHb were observed at ~10 s, ~30–50 s, and ~60 s post-stand, while O₂Hb levels were reduced at ~50 s, ~60 s, ~70–110 s, ~130 s, and ~140 s post-stand. No statistically significant group-level differences were observed based on antihypertensive medication use or frailty status. These findings demonstrate the utility of FDA in detecting subtle, time-dependent physiological variations during orthostatic challenge and underscore the value of continuous neurocardiovascular monitoring in assessing orthostatic tolerance in aging populations. Full article

Long QT syndrome (LQTS) presents a group of inheritable channelopathies with prolonged ventricular repolarization, leading to syncope, ventricular tachycardia, and sudden death. Differentiating LQTS genotypes is crucial for targeted management and treatment, yet conventional genetic testing remains costly and time-consuming. This study aims to improve the distinction between LQTS genotypes, particularly LQT3, through a novel electrocardiogram (ECG)-based approach. Patients with LQT3 are at elevated risk due to arrhythmia triggers associated with rest and sleep. Employing a database of genotyped long QT syndrome E-HOL-03-0480-013 ECG signals, we introduced two innovative parameterization techniques—area under the ECG curve and wave transformation into the unit circle—to classify LQT3 against LQT1 and LQT2 genotypes. Our methodology utilized single-lead ECG data with a 200 Hz sampling frequency. The support vector machine (SVM) model demonstrated the ability to discriminate LQT3 with a recall of 90% and a precision of 81%, achieving an F1-score of 0.85. This parameterization offers a potential substitute for genetic testing and is practical for low frequencies. These single-lead ECG data could enhance smartwatches’ functionality and similar cardiovascular monitoring applications. The results underscore the viability of ECG morphology-based genotype classification, promising a significant step towards streamlined diagnosis and improved patient care in LQTS. Full article

Inherited cardiac channelopathies are major causes of sudden cardiac death (SCD) in young people. Genetic testing is focused on the identification of single-nucleotide variants (SNVs) by Next-Generation Sequencing (NGS). However, genetically elusive cases can carry copy number variants (CNVs), which need specific detection tools. We underlie the utility of identifying CNVs by investigating the literature data and internally analyzing cohorts with CNVs in KCNQ1, KCNH2, SCN5A, and RYR2. CNVs were reported in 119 patients from the literature and 21 from our cohort. Young patients with CNVs in KCNQ1 show a Long QT (LQT) phenotype > 480 ms and a higher frequency of syncope. None of them had SCD. All patients with CNV in KCNH2 had a positive phenotype for QT > 480 ms. CNVs in SCN5A were represented by the Brugada pattern, with major cardiac events mainly in males. Conversely, adult females show more supraventricular arrhythmias. RYR2-exon3 deletion showed a broader phenotype, including left ventricular non-compaction (LVNC) and catecholaminergic polymorphic ventricular tachycardia (CPVT). Pediatric patients showed atrial arrhythmias and paroxysmal atrial fibrillation. Relatively higher syncope and SCA were observed in young females. The detection of CNVs can be of greater yield in two groups: familial channelopathies and patients with suspected Jervell and Lange-Nielsen syndrome or CPVT. The limited number of reported individuals makes it mandatory for multicentric studies to give future conclusive results. Full article

Purpose: Syncope remains a common medical problem. Recently, the role of dedicated syncope units and implantable loop recorders has emerged in the investigation of unexplained syncope. This study aims to investigate the possibilities for a more rational and targeted use of various diagnostic tools. Methods: In this retrospective single-center study, 196 patients with unexplained syncope were included between March 2019 and February 2023. Various diagnostic tools were utilized during the investigation, according to clinical judgement. Patients were retrospectively allocated into Group A (including those who, among other tests, underwent loop recorder insertion) and Group B (including patients investigated without loop recorder implantation). Data were compared with Group C, including patients assessed prior to syncope unit establishment. Results: There was no difference between Group A (n = 133) and Group B (n = 63) in the diagnostic yield (74% vs. 76%, p = 0.22). There were significant differences between Groups A and B regarding age (67.3 ± 16.9 years vs. 48.3 ± 19.1 years, p < 0.001) and cause of syncope (cardiogenic in 69% of Group A, reflex syncope in 77% of Group B, p < 0.001). Electrocardiography-based diagnosis occurred in 55% and 19% of Groups A and B, respectively (p < 0.001). The time to diagnosis was 4.2 ± 2.7 months in Group A and 7.5 ± 5.6 months in Group B (p < 0.001). In Group C, the diagnostic yield was 57.9% and the electrocardiography-based diagnostic yield was 18.3%. Conclusions: A selective use of loop recorders according to clinical and electrocardiographic characteristics increases the effectiveness of the structured syncope unit approach and further preserves financial resources. Full article

A heart with a borderline ventricle refers to a situation where there is uncertainty about whether the left or right underdeveloped ventricle can effectively support the systemic or pulmonary circulation with appropriate filling pressures and sufficient physiological reserve. Pediatric cardiologists often deal with congenital heart diseases (CHDs) associated with various degrees of hypoplasia of the left or right ventricles. To date, no specific guidelines exist, and surgical management may be extremely variable in different centers and sometimes even in the same center at different times. Thus, the choice between the single-ventricle or biventricular approach is always controversial. The aim of this review is to better define when “small is too small and large is large enough” in order to help clinicians make the decision that could potentially affect the patient’s entire life. Full article

Guidelines are important tools to guide the diagnosis and treatment of patients to improve the decision-making process of health professionals. They are periodically updated according to new evidence. Four new Guidelines in 2021, 2022 and 2023 referred to pediatric pacing and defibrillation. There are some relevant changes in permanent pacing. In patients with atrioventricular block, the heart rate limit in which pacemaker implantation is recommended was decreased to reduce too-early device implantation. However, it was underlined that the heart rate criterion is not absolute, as signs or symptoms of hemodynamically not tolerated bradycardia may even occur at higher rates. In sinus node dysfunction, symptomatic bradycardia is the most relevant recommendation for pacing. Physiological pacing is increasingly used and recommended when the amount of ventricular pacing is presumed to be high. New recommendations suggest that loop recorders may guide the management of inherited arrhythmia syndromes and may be useful for severe but not frequent palpitations. Regarding defibrillator implantation, the main changes are in primary prevention recommendations. In hypertrophic cardiomyopathy, pediatric risk calculators have been included in the Guidelines. In dilated cardiomyopathy, due to the rarity of sudden cardiac death in pediatric age, low ejection fraction criteria were demoted to class II. In long QT syndrome, new criteria included severely prolonged QTc with different limits according to genotype, and some specific mutations. In arrhythmogenic cardiomyopathy, hemodynamically tolerated ventricular tachycardia and arrhythmic syncope were downgraded to class II recommendation. In conclusion, these new Guidelines aim to assess all aspects of cardiac implantable electronic devices and improve treatment strategies. Full article

Syncope is a highly prevalent clinical condition characterized by a rapid, complete, and brief loss of consciousness, followed by full recovery caused by cerebral hypoperfusion. This symptom carries significance, as its potential underlying causes may involve the heart, blood pressure, or brain, leading to a spectrum of consequences, from sudden death to compromised quality of life. Various factors contribute to syncope, and adhering to a precise diagnostic pathway can enhance diagnostic accuracy and treatment effectiveness. A standardized initial assessment, risk stratification, and appropriate test identification facilitate determining the underlying cause in the majority of cases. New technologies, including artificial intelligence and smart devices, may have the potential to reshape syncope management into a proactive, personalized, and data-centric model, ultimately enhancing patient outcomes and quality of life. This review addresses key aspects of syncope management, including pathogenesis, current diagnostic testing options, treatments, and considerations in the geriatric population. Full article

Syncope is a challenging problem in the emergency department (ED) as the available risk prediction tools have suboptimal predictive performances. Predictive models based on machine learning (ML) are promising tools whose application in the context of syncope remains underexplored. The aim of the present study was to develop and compare the performance of ML-based models in predicting the risk of clinically significant outcomes in patients presenting to the ED for syncope. We enrolled 266 consecutive patients (age 73, IQR 58–83; 52% males) admitted for syncope at three tertiary centers. We collected demographic and clinical information as well as the occurrence of clinically significant outcomes at a 30-day telephone follow-up. We implemented an XGBoost model based on the best-performing candidate predictors. Subsequently, we integrated the XGboost predictors with knowledge-based rules. The obtained hybrid model outperformed the XGboost model (AUC = 0.81 vs. 0.73, p < 0.001) with acceptable calibration. In conclusion, we developed an ML-based model characterized by a commendable capability to predict adverse events within 30 days post-syncope evaluation in the ED. This model relies solely on clinical data routinely collected during a patient’s initial syncope evaluation, thus obviating the need for laboratory tests or syncope experienced clinical judgment. Full article

Background: Sarcopenia, delayed blood pressure (BP) recovery following standing, and orthostatic hypotension (OH) pose significant clinical challenges associated with ageing. While prior studies have established a link between sarcopenia and impaired BP recovery and OH, the underlying haemodynamic mechanisms remain unclear. Methods: We enrolled 107 participants aged 50 and above from a falls and syncope clinic, conducting an active stand test with continuous non-invasive haemodynamic measurements. Hand grip strength and five-chair stand time were evaluated, and muscle mass was estimated using bioelectrical impedance analysis. Participants were categorised as non-sarcopenic or sarcopenic. Employing mixed-effects linear regression, we modelled the effect of sarcopenia on mean arterial pressure and heart rate after standing, as well as Modelflow^®-derived parameters such as cardiac output, total peripheral resistance, and stroke volume, while adjusting for potential confounders. Results: Sarcopenia was associated with diminished recovery of mean arterial pressure during the 10–20 s period post-standing (β −0.67, p < 0.001). It also resulted in a reduced ascent to peak (0–10 s) and recovery from peak (10–20 s) of cardiac output (β −0.05, p < 0.001; β 0.06, p < 0.001). Furthermore, sarcopenia was associated with attenuated recovery (10–20 s) of total peripheral resistance from nadir (β −0.02, p < 0.001) and diminished recovery from peak (10–20 s) of stroke volume (β 0.54, p < 0.001). Notably, heart rate did not exhibit a significant association with sarcopenia status at any time interval post-standing. Conclusion: The compromised BP recovery observed in sarcopenia appears to be driven by an initial reduction in the peak of cardiac output, followed by attenuated recovery of cardiac output from its peak and total peripheral resistance from its nadir. This cardiac output finding seems to be influenced by stroke volume rather than heart rate. Possible mechanisms for these findings include cardio-sarcopenia, the impact of sarcopenia on the autonomic nervous system, and/or the skeletal muscle pump. Full article

Double-outlet left ventricle (DOLV) is an abnormal ventriculo-arterial connection characterized by the origin of both great arteries from the morphological left ventricle. The aim of our paper is to describe the morphological and imaging features of DOLV and to assess the prevalence of the associated malformations and their surgical outcomes. METHODS From 2011 to 2022, we retrospectively reviewed the electronic case records of patients diagnosed with DOLV at the Bambino Gesu Children’s Hospital. A systematic search was developed in MEDLINE, Web of Science, and EMBASE databases to identify reports assessing the morphology and outcomes of DOLV between 1975 and 2023. RESULTS: Over a median follow-up of 9.9 years (IQR 7.8–11.7 y), four cases of DOLV were identified at our institution. Two patients were diagnosed with (S,D,D) DOLV subaortic VSD and pulmonary stenosis (PS): one patient had (S,D,D) DOLV with doubly committed VSD and hypoplastic right ventricle, and another patient had (S,D,L) DOLV with subaortic VSD and PS (malposition type). Pulmonary stenosis was the most commonly associated lesion (75%). LITERATURE REVIEW: After systematic evaluation, a total of 12 reports fulfilled the eligibility criteria and were included in our analysis. PS or right ventricular outflow tract obstruction was the most commonly associated lesion (69%, 95% CI 62–76%). The most common locations of VSD were subaortic (pooled prevalence: 75%, 95% CI 68–81), subpulmonary (15%, 95% CI 10–21), and doubly committed (7%, 95% CI 4–12). The position of the great arteries showed that d-transposition of the aorta was present in 128 cases (59% 95% CI 42–74), and l-transposition was present in 77 cases (35%, 95% CI 29–43). Full article

The heart and seizures are closely linked by an indissoluble relationship that finds its basis in the cerebral limbic circuit whose mechanisms remain largely obscure. The differential diagnosis between seizures and syncopes has always been a cornerstone of the collaboration between cardiologists and neurologists and is renewed as a field of great interest for multidisciplinary collaboration in the era of the diffusion of prolonged telemonitoring units. The occurrence of ictal or post-ictal arrhythmias is currently a cause of great scientific debate with respect to the role and risks that these complications can generate (including sudden unexpected death in epilepsy). Furthermore, the study of epileptic seizures and the arrhythmological complications they cause (during and after seizures) also allows us to unravel the mechanisms that link them. Finally, intercritical arrhythmias may represent great potential in terms of the prevention of cardiological risk in epileptic patients as well as in the possible prediction of the seizures themselves. In this paper, we review the pertaining literature on this subject and propose a scheme of classification of the cases of arrhythmia temporally connected to seizures. Full article

Although very common, the precise mechanisms that explain the symptomatology of neuroendocrine syncope (NES) remain poorly understood. This disease, which can be very incapacitating, manifests itself as a drop in blood pressure secondary to vasodilation and/or extreme slowing of heart rate. As studies continue, the involvement of the adenosinergic system is becoming increasingly evident. Adenosine, which is an ATP derivative, may be involved in a large number of cases. Adenosine acts on G protein-coupled receptors with seven transmembrane domains. A₁ and A_2A adenosine receptor dysfunction seem to be particularly implicated since the activation leads to severe bradycardia or vasodilation, respectively, two cardinal symptoms of NES. This mini-review aims to shed light on the links between dysfunction of the adenosinergic system and NHS. In particular, signal transduction pathways through the modulation of cAMP production and ion channels in relation to effects on the cardiovascular system are addressed. A better understanding of these mechanisms could guide the pharmacological development of new therapeutic approaches. Full article