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BACKGROUND: Bradycardia is more common among well-trained athletes than in the general population, but the association with pacemaker implantations is less known. We investigated associations of endurance training with incidence of bradycardia and pacemaker implantations, including sex differences and long-term outcome, in a cohort of endurance trained individuals. METHODS: All Swedish skiers who completed >1 race in the cross-country skiing event Vasaloppet between 1989 and 2011 (n=209 108) and a sample of 532 290 nonskiers were followed until first event of bradycardia, pacemaker implantation, or death, depending on end point. The Swedish National Patient Register was used to obtain diagnoses. Cox regression was used to investigate associations of number of completed races and finishing time in Vasaloppet with incidence of bradycardia and pacemaker implantations. In addition, Cox regression was used to investigate associations of pacemaker implantations with death in skiers and nonskiers. RESULTS: Male skiers had a higher incidence of bradycardia (adjusted hazard ratio [aHR], 1.19 [95% CI, 1.05-1.34]) and pacemaker implantations (aHR, 1.17 [95% CI, 1.04-1.31]) compared with male nonskiers. Those who completed the most races and had the best performances exhibited the highest incidence. For female skiers in Vasaloppet, the incidence of bradycardia (aHR, 0.98 [95% CI, 0.75-1.30]) and pacemaker implantations (aHR, 0.98 [95% CI, 0.75-1.29]) was not different from that of female nonskiers. The indication for pacemaker differed between skiers and nonskiers, with sick sinus syndrome more common in the former and third-degree atrioventricular block in the latter. Skiers had lower overall mortality rates than nonskiers (aHR, 0.16 [95% CI, 0.15-0.17]). There were no differences in mortality rates by pacemaker status among skiers. CONCLUSIONS: In this study, male endurance skiers had a higher incidence of bradycardia and pacemaker implantations compared with nonskiers, a pattern not seen in women. Among male skiers, those who completed the most races and had the fastest finishing times had the highest incidence of bradycardia and pacemaker implantations. Within each group, mortality rates did not differ in relation to pacemaker status. These findings suggest that bradycardia associated with training leads to a higher risk for pacemaker implantation without a detrimental effect on mortality risk.
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To compare the efficacy and safety of bedside ultrasound-guided and fluoroscopy-guided transvenous cardiac temporary pacing in the treatment of bradyarrhythmia in children. Children treated by temporary intravenous cardiac pacing from January 2016 to June 2023 in Hunan Provincial Children's Hospital were enrolled, and the characteristics and data of the cases were summarized. Patients were divided into bedside ultrasound-guided group (ultrasound group) and fluoroscopy-guided group (fluoroscopy group) according to the implantation guidance methods. The efficacy, safety, and incidence of complications in children were compared, and follow-up analysis was carried out. A total of 30 children were enrolled, including 18 males and 12 females, with a median age of 5.5 (2.9, 10.0) years and a median weight of 18.7 (12.7, 32.7) kg. The most common primary diseases were fulminant myocarditis (13/30 cases) and congenital high-grade AVB (10/30 cases). Among them, the proportion of congenital high AVB in the fluoroscopy group was significantly higher than that in the ultrasound group, and the difference was statistically significant (p = 0.007). The implantation process was successful in all 30 children. From the time of pacing decision to implantation, the median time of ultrasound group was 56 (30, 60) min and that of fluoroscopy group was 154 (78,180) min, with a statistically significant difference (P < 0.001). A total of 5 cases developed complications. There was no statistically significant difference between the two groups (P > 0.05). Compared with traditional fluoroscopic temporary pacing, bedside ultrasound-guided temporary pacing technology can effectively shorten the operation time and reduce the occurrence of complications and has become a better choice for children's emergency and critical care treatment. The right internal jugular vein is preferred for intravenous implantation.
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Iron deficiency anemia is an important problem among pregnant women, and intravenous (IV) iron infusions have been increasingly used. Whether fetal monitoring is required during infusion has been debated, with a recent guideline by Hematologists recommending against such. We report two cases of fetal bradycardia after iron isomaltoside (IIM), in women with otherwise good maternal and fetal health. Both developed dyspnea with desaturation minutes from infusion, followed by persistent fetal bradycardia. Both underwent category 1 CS, with cord arterial pH of 7.08 and 6.94 respectively. Upon literature review, only three case reports on fetal bradycardia in IV iron were identified. For older IV iron formulations, a case was reported after IV dextran test dose, while two cases after ferric gluconate were reported. For the new formulation IIM, only one case was reported so far, but in a woman with Crohn's disease and intrauterine growth restriction. IV iron in pregnancy carries risk of anaphylactic or hypersensitivity reactions, even with the newest formulations and in women with good maternal and fetal health. While rarely reported so far, fetal bradycardia is a possible consequence, commonly preceded by respiratory symptoms. Fetal monitoring should therefore be considered during infusion.
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Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is the most common form of autoimmune encephalitis, presenting with various psychiatric manifestations, including behavioral and cognitive impairments, movement disorders, decreased consciousness, dysphasia, seizures, and autonomic dysfunction. Autonomic dysfunction may involve hyperthermia, apnea, hypotension, tachycardia, and life-threatening manifestations of sinus node dysfunction (SND), such as bradycardia, sinus pause or arrest, and asystole. The severity and significance of SND are critical, as it is not uncommon for these patients to progress into asystolic cardiac arrest, potentially contributing to morbidity and mortality. Accordingly, we present the case of an 18-year-old female with anti-NMDAR encephalitis who experienced multiple episodes of sinus pause/arrest and asystolic cardiac arrest, achieving a return of spontaneous circulation after successful CPR in all instances, ultimately requiring permanent pacemaker implantation. Additionally, we performed a literature review and analyzed 23 similar anti-NMDAR encephalitis cases with SND manifestations, including sinus pause/arrest or asystolic cardiac arrest, to identify common risk factors and describe management strategies and outcomes. Moreover, we investigated the potential association between teratoma and permanent pacemaker use in SND.
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A primigravida at 36 weeks with gestational diabetes mellitus and hypothyroidism and no prior chronic medical illness was admitted for safe confinement. A cesarean section was required to deliver the baby with breech presentation complicated by a slow progression of labor. Asymptomatic sinus bradycardia with a heart rate of 40 per minute was observed during the induction of anesthesia. Before bupivacaine administration for spinal anesthesia, she was administered pantoprazole 40 mg and ondansetron 4 mg intravenously. ECG recording showed a type 1 Mobitz second-degree heart block. Follow-up ECG showed progression of heart block to type 2 Mobitz second-degree heart block. The second-degree heart block persisted for 16 hours, during which the patient was asymptomatic, and the ventricular rate was maintained at a range of 60-80 per minute. After normalization of rhythm, the patient was observed in the ICU. She received another dose of ondansetron 4 mg intravenously for vomiting, and the heart block recurred. The rhythm disturbance was attributed to ondansetron. Her rhythm normalized after 36 hours, and she was subsequently discharged home three days later.
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Background: Observational studies have shown that heart rate (HR), heart rate variability (HRV), P-wave terminal force, P-wave duration, T-wave amplitude and PR interval are associated with risk factors for atrial fibrillation (AF) or bradycardia. Arrhythmias are associated with many causes of hospitalization. However, observational studies are susceptible to confounding factors that have not yet been identified. The objective of this study was to clarify the causal relationships by Mendelian randomization analysis. Methods: We conducted a two-sample and multivariate Mendelian randomization (MVMR) analysis using genome-wide association study (GWAS) data from a European population to assess the total and direct causal effects of HR, three HRV traits, P-wave terminal force, P-wave duration, T-wave top amplitude in five-lead modes, and the PR interval on the risk of AF (N=191,205), bradycardia (N=463,010), and supraventricular tachycardia (SVT) (N=463,010). Results: The results of the univariate MR analysis revealed the following significant causal effects: the higher the genetically predicted PR interval, the lower the risk of AF; the higher the HR and T-wave top amplitude (aVR leads and V3 + V4 + aVL leads), the lower the risk of bradycardia; and the higher HR and the lower PR interval, the higher the risk of SVT. The multivariate MR results indicated that the HRV_standard deviation of the normal-to-normal (SDNN) interval had an independent causal effect on the risk of AF [odds ratio (OR): 0.515; 95% confidence interval (CI): 0.278-0.954; P=0.03], and the T-wave top amplitude in the aVR leads (OR: 0.998; 95% CI: 0.996-0.999; P<0.001) and the HRV_SDNN (OR: 0.988; 95% CI: 0.976-1.000; P=0.045) had independent causal effects on the risk of bradycardia. Conclusions: The HRV_SDNN had an independent causal effect on AF, while the HRV_SDNN and T-wave top amplitude in the aVR leads had independent causal effects on bradycardia, which suggests that some of the electrocardiographic parameters have preventive effects on the incidence of AF and bradycardia.
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Neonatal lupus may be associated with severe cardiac conduction problems, including high-degree or complete atrioventricular (AV) block, necessitating immediate pacemaker implantation during the neonatal period. However, cardiac manifestations of neonatal lupus may extend beyond AV block. Our case was a full-term female neonate, who presented with fetal arrhythmia and bradycardia with a heart rate of approximately 70-75 beats per minute after birth. Neonatal lupus was diagnosed later due to positive maternal and neonatal anti-SSA/Ro antibody. High-degree AV block was considered initially but bigeminy premature atrial contractions (PACs) with block was confirmed through a detailed evaluation of an electrocardiogram, which demonstrated unfixed PP intervals and fixed RR intervals. Atrial tachycardia (AT) developed when the neonate was 23 days old. The key point that differentiates high-degree AV block from PACs with block is the PP interval. The PP interval is fixed in high-degree AV block and unfixed in PACs with block. Careful differential diagnosis is required in neonates with bradycardia because it may lead to very different management. Our case presents a good illustration of why these arrhythmias need to be differentiated. Furthermore, our case may be the first of neonatal lupus with AT.
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Seldom are reports of phase 4 block or bradycardia-dependent conduction block in atrial tissue found in the literature. Here, we describe the case of a patient with sick sinus syndrome with Torsade de Pointes who, following the implantation of a double-chamber implantable cardioverter defibrillator, developed intra-atrial bradycardia-dependent conduction block. The patient's optimal pacing parameters were achieved by raising the rate.
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BACKGROUND: Fludarabine is a chemotherapeutic agent with lymphodepleting effects that is increasingly used as part of a conditioning regimen prior to allogeneic stem cell transplantation. Fludarabine is generally considered a relatively safe medication with only rare cases of cardiotoxic side effects. CASE PRESENTATION: Here, we present a case of a 30-year-old woman who was undergoing conditioning for a haploidentical cell transplantation for treatment of Fanconi anemia with a 5-day course of daily fludarabine infusion. After her second fludarabine infusion, she was noted to have ectopic atrial bradycardia that resolved with supportive therapy and completion of fludarabine infusion. CONCLUSION: We report the first case of ectopic atrial bradycardia associated with fludarabine. Although rare and transient, clinicians should recognize this rare cardiotoxic side effect of fludarabine.
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Key Clinical Message: The purpose of this case report is to reveal one of the cardiovascular side effects of favipiravir, sinus bradycardia. Abstract: Favipiravir has emerged as a potential treatment for COVID-19, with its antiviral properties showing promise in inhibiting viral replication. However, concerns regarding its safety profile, particularly its cardiac adverse effects, remain a subject of debate. We present the case of a 58-year-old man with a history of diabetes mellitus and chronic obstructive pulmonary disease who developed bradycardia following treatment with favipiravir for COVID-19 pneumonia. Despite being asymptomatic, the patient exhibited sinus bradycardia, which resolved upon discontinuation of favipiravir. Favipiravir has been associated with QT prolongation and sinus bradycardia, though the exact mechanisms remain unclear. Our case adds to the growing body of evidence highlighting the potential cardiac complications of favipiravir therapy in COVID-19 patients. Further research is warranted to clarify the underlying mechanisms and optimize patient management strategies. Clinicians should be cautious for cardiac adverse events when prescribing favipiravir for COVID-19 treatment, especially in patients with preexisting cardiac conditions. Continued research is essential to ensure the safe and effective use of favipiravir in the management of COVID-19.
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BRASH (bradycardia, renal dysfunction, atrioventricular node blockade, shock, and hyperkalemia) syndrome is a recently recognized clinical process that can be fatal if not adequately and promptly treated. As such, it is important for clinicians to recognize the syndrome. This case demonstrates an example of BRASH syndrome in a 73-year-old patient with heart failure occurring after initiation of dapagliflozin, a drug not previously associated with this phenomenon in the literature. Given the increasingly appreciated clinical utility of sodium-glucose cotransporter-2 (SGLT-2) inhibitors, prescribers must respect their potential side effects in patients with underlying comorbidities and remember the importance of re-evaluating renal function after initiation of these medications. Here, we review the pathophysiology of BRASH, the renal effects of SGLT-2 inhibitors, and the importance of educating patients on volume management and diuretic dose titration at home.
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Isolated cardiac sarcoidosis is a rare phenomenon of systemic sarcoidosis, with presentation ranging from asymptomatic to sudden cardiac death. Controversy exists on diagnostic and therapeutic options, creating an ongoing challenge for clinicians in providing patient care. A 79-year-old male presented status post looposcopy and interval ureteral stent replacement with sinus bradycardia and high-degree atrioventricular block. A comprehensive examination was performed that conclusively ruled out common etiologies of atrioventricular block, including coronary artery disease, electrolyte abnormalities, and medications. This prompted an investigation using advanced cardiac imaging modalities that demonstrated cardiac sarcoidosis. Computed tomography of the chest was negative for lymphadenopathy or infiltrates indicative of pulmonary involvement. The lack of extracardiac manifestations, in combination with imaging findings, led to a probable diagnosis of isolated cardiac sarcoidosis. The patient underwent biventricular implantable cardioverter defibrillator placement and was started on oral corticosteroids.
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BACKGROUND: Half of pediatric in-hospital cardiopulmonary resuscitation (CPR) events have an initial rhythm of non-pulseless bradycardia with poor perfusion. Our study objectives were to leverage granular data from the ICU-RESUScitation (ICU-RESUS) trial to: (1) determine the association of early epinephrine administration with survival outcomes in children receiving CPR for bradycardia with poor perfusion; and (2) describe the incidence and time course of the development of pulselessness. METHODS: Prespecified secondary analysis of ICU-RESUS, a multicenter cluster randomized trial of children (< 19 years) receiving CPR in 18 intensive care units in the United States. Index events (October 2016-March 2021) lasting ≥ 2 min with a documented initial rhythm of bradycardia with poor perfusion were included. Associations between early epinephrine (first 2 min of CPR) and outcomes were evaluated with Poisson multivariable regression controlling for a priori pre-arrest characteristics. Among patients with arterial lines, intra-arrest blood pressure waveforms were reviewed to determine presence of a pulse during CPR interruptions. The temporal nature of progression to pulselessness was described and outcomes were compared between patients according to subsequent pulselessness status. RESULTS: Of 452 eligible subjects, 322 (71%) received early epinephrine. The early epinephrine group had higher pre-arrest severity of illness and vasoactive-inotrope scores. Early epinephrine was not associated with survival to discharge (aRR 0.97, 95%CI 0.82, 1.14) or survival with favorable neurologic outcome (aRR 0.99, 95%CI 0.82, 1.18). Among 186 patients with invasive blood pressure waveforms, 118 (63%) had at least 1 period of pulselessness during the first 10 min of CPR; 86 (46%) by 2 min and 100 (54%) by 3 min. Sustained return of spontaneous circulation was highest after bradycardia with poor perfusion (84%) compared to bradycardia with poor perfusion progressing to pulselessness (43%) and bradycardia with poor perfusion progressing to pulselessness followed by return to bradycardia with poor perfusion (62%) (p < 0.001). CONCLUSIONS: In this cohort of pediatric CPR events with an initial rhythm of bradycardia with poor perfusion, we failed to identify an association between early bolus epinephrine and outcomes when controlling for illness severity. Most children receiving CPR for bradycardia with poor perfusion developed subsequent pulselessness, 46% within 2 min of CPR onset.
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Bradicardia , Reanimación Cardiopulmonar , Epinefrina , Humanos , Epinefrina/administración & dosificación , Epinefrina/uso terapéutico , Reanimación Cardiopulmonar/métodos , Reanimación Cardiopulmonar/estadística & datos numéricos , Masculino , Femenino , Bradicardia/tratamiento farmacológico , Bradicardia/terapia , Preescolar , Niño , Lactante , Adolescente , Unidades de Cuidados Intensivos/estadística & datos numéricos , Unidades de Cuidados Intensivos/organización & administraciónRESUMEN
Introduction: Although terlipressin is known to cause bradycardia, this adverse effect is usually described in association with hypertension and is considered a benign compensatory response mediated by arterial baroreceptors. Cardiac monitoring for patients receiving terlipressin is not routinely recommended. Case Presentation: A 77-year-old female patient with no history of coronary artery disease and no other coexisting risk factors for cardiac arrhythmias or conduction disturbances was admitted to intensive care unit with severe cholangitis, complicated by variceal bleeding. She developed severe sinus bradycardia following the use of terlipressin, which was associated with significant hypotension that required the infusion of norepinephrine. The bradycardia occurred again when terlipressin therapy was reattempted. Conclusion: Vasopressin is known to sensitize baroreceptor reflexes by a central mechanism though its actions on V1a receptors in the area postrema, and we speculate that vasopressin analogues such as terlipressin may act in the same manner. That this effect is not widely described in terlipressin safety literature may be due to the overall younger age range of the trial population. This raises the possibility that cardiac monitoring may be warranted for elderly patients receiving terlipressin.
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Amitraz poisoning is being increasingly seen in clinical practice, presenting physicians with challenges due to its rapidity of onset of severe clinical features, its similarity with organophosphate poisoning and the absence of specific antidotes. Early initiation and appropriate treatment are vital for favourable outcomes. Our case report is of a 40-year-old male who presented to us with grave clinical features following deliberate ingestion of Amitraz in a suicidal attempt. On arrival, he had bradycardia, hypotension, respiratory depression, and altered sensorium. Immediate administration of atropine stabilised his vital signs. Laboratory investigations revealed uncommon electrolyte imbalances, which were promptly corrected. The patient received supportive care in the intensive care unit (ICU), regained consciousness within three days, and was discharged after a week of hospitalisation. Despite the rapid onset and severity of symptoms caused by Amitraz poisoning, early intervention and supportive care can lead to a full recovery. This case underscores the importance of promptly recognising Amitraz poisoning and initiating treatment, its similarity with organophosphate poisoning and the role of atropine. Further research is needed to establish comprehensive management guidelines for tackling this emerging poisoning hazard.
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Organophosphorus flame retardants (OPFRs) such as triphenyl phosphate (TPHP) and tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) were reported to impair cardiac function in fish. However, limited information is available regarding their cardiotoxic mechanisms. Using rare minnow (Gobiocypris rarus) as a model, we found that both TPHP and TDCIPP exposures decreased heart rate at 96 h postfertilization (hpf) in embryos. Atropine (an mAChR antagonist) can significantly attenuate the bradycardia caused by TPHP, but only marginally attenuated in TDCIPP treatment, suggesting that TDCIPP-induced bradycardia is independent of mAChR. Unlike TDCIPP, although TPHP-induced bradycardia could be reversed by transferring larvae to a clean medium, the inhibitory effect of AChE activity persisted compared to 96 hpf, indicating the existence of other bradycardia regulatory mechanisms. Transcriptome profiling revealed cardiotoxicity-related pathways in treatments at 24 and 72 hpf in embryos/larvae. Similar transcriptional alterations were also confirmed in the hearts of adult fish. Further studies verified that TPHP and TDCIPP can interfere with Na+/Ca2+ transport and lead to disorders of cardiac excitation-contraction coupling in larvae. Our findings provide useful clues for unveiling the differential cardiotoxic mechanisms of OPFRs and identifying abnormal Na+/Ca2+ transport as one of a select few known factors sufficient to impair fish cardiac function.
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Cardiotoxicidad , Cyprinidae , Retardadores de Llama , Animales , Retardadores de Llama/toxicidad , Embrión no Mamífero/efectos de los fármacos , Compuestos Organofosforados/toxicidad , Organofosfatos/toxicidadRESUMEN
Cardioneuroablation has emerged as a potential alternative to cardiac pacing in selected cases with vasovagal reflex syncope, extrinsic vagally induced sinus bradycardia-arrest or atrioventricular block. The technique was first introduced decades ago, and its use has risen over the past decade. However, as with any intervention, proper patient selection and technique are a prerequisite for a safe and effective use of cardioneuroablation therapy. This document aims to review and interpret available scientific evidence and provide a summary position on the topic.
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Intravenous rapid injection of fentanyl causes respiratory depression (severe apneas), leading to sudden death, which constitutes the deadliest drug reaction among overdoses of synthetic opioids. Here we asked whether acute inhalation of overdose fentanyl would also result in similar respiratory failure and death. The anesthetized and spontaneously breathing rats with tracheal cannulation were exposed to aerosolized fentanyl at 100â¯mg/m3 (FNTH) or 30â¯mg/m3 (FNTL) for 10â¯min. Minute ventilation (VE), electromyography (EMG) of the internal and external intercostal muscles and thyroarytenoid muscles (EMGII, EMGEI, and EMGTA), heart rate and arterial blood pressure were recorded. During the exposure, FNTH and FNTL immediately triggered bradypnea (40â¯% reduction, p < 0.05) with TE prolonged and then gradually decreased VE by 40â¯% (P < 0.05) after a brief VE recovery. The initial TE prolongation (apneas) were characterized by the cessation of EMGEI activity with enhanced tonic discharges of EMGTA and EMGII. After termination of the exposure, the cardiorespiratory responses to FNTL returned to the baseline values 30â¯min later, while those to FNTH were greatly exacerbated (P < 0.05), leading to ventilatory and cardiac arrest occurred 16.4 ± 4.7â¯min and 19.3 ± 4.5â¯min respectively after the onset of FNTH. The ventilatory arrest was featured by cessation of both EMGEI and EMGII and augmentation of tonic EMGTA. Our results suggest that acute exposure to an overdose of fentanyl aerosol leads to death through initially inducing a brief central and upper airway obstructive apnea as well as chest wall rigidity followed by gradual severe hypoventilation, bradycardia and hypotension, and eventual cardiorespiratory arrest in anesthetized rats.